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Figure 1. Mr. DNA’s lesson from Jurassic Park (Spielberg, 1993, Universal Pictures): the mosquito, the amber, and the frog DNA that filled the holes. Still from the film, YouTube embed.

Later in the film, the fossil hunter Alan Grant turns over a piece of eggshell in the grass. It is hatched, and empty. The park made every dinosaur female, so none should breed. “Life found a way,” Grant says. One of the frog’s instructions let an animal switch from female to male. The dinosaurs’ cells could not tell which letters came from a frog. They read all of it and followed all of it.

Some of the cartoon is true: DNA is a code, and a cell builds a living thing by reading it. The amber is not. In moa bones, a short stretch of DNA has a half-life of about 521 years: after that long, half of it has broken apart. The oldest DNA found so far is about two million years old, and the last dinosaurs died sixty-six million years ago. Living DNA has no frog in it, but it has a backup. Every letter is stored twice, once as itself and once as its partner on the facing strand: T always across from A, C always across from G (Figure 2).

Figure 2. DNA as a museum model: two strands twisted together, every rung a pair of letters. Naturalis Biodiversity Center, Leiden. Photograph by Henk Caspers/Naturalis (2014), Wikimedia Commons, CC BY-SA 3.0.

A phone keyboard does the frog’s job every day. Someone types “see you at the,” and predictive text fills the blank with “gym.” The word fits the sentence. It is not the one they meant. The same phone catches slips too: type “teh,” and a red squiggle appears under it. Cells have a red squiggle of their own. Each time a cell copies its DNA, a crew of proteins checks the new copy against the old one. Only about one wrong letter in a billion gets through.

That crew is built from recipes in the genome, the cookbook every cell keeps, like any other protein. In some families, one of those recipes is broken from birth. Wrong letters can slip through, and colon cancer may come years early. The condition is called Lynch syndrome. About one person in three hundred carries it, most without knowing.

At your next checkup, the clipboard form will ask about family history: a box for each disease, a line for the relative’s age. Watch for three relatives with colon or uterine cancer, across two generations, one of them before fifty. That pattern points to Lynch syndrome, and a genetic test can find it. Someone I know learned she had rectal cancer in her late forties. Her son had his first colonoscopy at thirty-six, nine years before most Americans start. For a carrier, the test can move the first colonoscopy a decade or more earlier, but how do a few extra wrong letters turn into cancer?

What the Inspector Catches

The camera sweeps in low over an empty football field, grass catching early light. The shot opens a second film, this one about real DNA. Imagine the voice that follows as something like Morgan Freeman’s, calm and certain, the voice that says what is real.

Narrator: What does DNA look like? It is a chain of small repeating units called nucleotides. Each one carries a single base, one of four, written T, C, G or A. In this story, each nucleotide is a sprite.

The grass at the edges of the frame blurs. Its color deepens and its outlines sharpen, until the picture looks hand drawn.

The sprites appear first: thumb-sized wingless creatures with a faint shimmer across their skin, pastel one second and rainbow-bright the next. Their eyes burn a rich, liquid amber, the warmth of trapped sunlight. Each one holds a single glowing, magnetic bead pressed close to its chest, stamped with one of four letters: T, C, G or A (Figure 3).

Figure 3. The four kinds of sprite, one for each letter: T, C, G and A, each holding its bead. Drawn for this piece, using a sprite illustration from Reverso Dictionary only as a reference: no wings, new colors, and the beads added.

The field holds six billion sprites. A single copy of human DNA has about three billion pairs of letters, and every pair takes a sprite from each strand. Each sprite holds hands with its neighbors along its own strand, end to end down the field. Two strands lean into each other and twist over and over, the way two vines climb together. That twist is the one biology textbooks draw, the double helix. Across it, each sprite holds one partner, the same pairs as the backup: T with A, C with G.

Watching over the sprites is an imp, and it looks nothing like them. It is low to the ground and broad-shouldered, its face taken over by a nose too big for it, a nose that never stops twitching. An imp is not a nucleotide and never was. It stands for an enzyme, a piece of the cell’s machinery that acts on the code rather than being part of it. The imp lifts a tiny megaphone and calls down the field, “INSPECTION!”

One of the two strands is brand new, copied from the other a moment ago. Most of the walk is uneventful: T holding A, C holding G, pair after pair. Then, somewhere past midfield, the imp’s nose twitches harder and stops.

A T has ended up paired with a C. A wrong pair gives off a smell, faint but unmistakable: a skunk that got too close. In a cartoon the smell would earn its own wavy green cloud, the field’s red squiggle. The imp follows its nose straight to the wrong pair and pries it apart. The beads were never locked, only resting uneasily against each other. Within moments the real partner drifts into place, the A the T should have had all along. This time there is a click, sharp as a snap, and a jolt runs through the imp’s fingers. The imp moves on, nose twitching, for the next few billion yards.

Narrator: Real pairs are held together by hydrogen bonds, weak pulls between the bases, a little like the pull of the beads’ magnets. A T and a C fit badly and hold weakly, so a pair like that one stays loose. The smell is invented. The repair is not. Copying makes slips far more often than the finished strand shows, because mismatch repair proteins follow the copying machinery, find loose pairs, and fix them. Four genes hold most of the recipes for that crew: MLH1, MSH2, MSH6 and PMS2.

A slip the imp misses stays put, and the cell reads it as if it were right, the way a friend reads “gym” in a text without a second look. The imp would have let the park’s frog letters pass too, since each was paired with its right partner and nothing smelled. In some families, the imp can break.

What the Inspector Lets Through

In 1895, a seamstress told a Michigan pathologist she would die of cancer, because so many in her family had. She did, of cancer of the uterus. The pathologist, Aldred Warthin, traced her relatives and in 1913 published them as “Family G.” In the 1960s, Henry Lynch found the family again: more than 650 members. Ninety-five of them had cancer. Lynch syndrome is named for him.

Family G had a broken inspector. A carrier is born with a broken copy of a repair gene from one parent and a working copy from the other. One working copy is enough to run the crew, the way a spare key still opens the door when the first one is lost. The trouble starts in a single cell, say in the lining of the colon, that loses the working copy too. The geneticist Alfred Knudson worked out this two-hit pattern in 1971, for a cancer of the eye in young children. The first hit is inherited. The second happens in one cell, years later.

From that cell on, the squiggle stays off. Typos pile up everywhere, and fastest in runs of repeats: CACACACA, or ten A’s in a row. Copying slips on a run the way a thumb does on “nooooo,” which comes out with a different number of o’s each time. A working inspector catches the extra or missing unit. A broken one lets it stand, so the runs in a tumor end up longer or shorter than the same runs in the person’s blood. That stutter is called microsatellite instability, or MSI.

Some of those runs lie in genes that tell a cell when to stop dividing. One of them, TGFBR2, has a run of ten A’s. Researchers found that 100 of 111 colon tumors with MSI had gained or lost an A in that run. Every letter after the slip is read out of step, the stop order never arrives, and the cell keeps dividing.

Not every carrier gets cancer. A large follow-up tracked 3,119 carriers up to age seventy-five. By then, about 46 in 100 with a broken MLH1 had colon cancer. With a broken MSH6, about 15 in 100 did. For women with a broken MSH2, uterine cancer reached about 57 in 100. In one family, a mother with colon cancer at fifty and an aunt who never had it can carry the same broken copy. One relative who stayed well proves nothing for the rest. Why some carriers get cancer young and others never do is still being studied. What is known is that the typos leave a trail in the tumor.

What the Inspector Leaves Behind

A colon tumor comes out in surgery, and a slice of it goes to the pathology lab. Two tests follow that trail. One counts the stutter: it measures a handful of repeat runs in the tumor against the same runs in normal tissue. The other stains the four repair proteins brown. A protein that leaves no brown points to the gene that broke (Figure 4).

Figure 4. A tumor of the uterine lining stained for MLH1. The healthy cells around it turn brown, but the tumor cells stay blue: the inspector is missing there. Photograph by Mikael Häggström (2022), Wikimedia Commons, CC0.

Guidelines now call for testing every colon and uterine tumor this way, so Lynch syndrome can turn up in a family whose form shows nothing. A stutter does not always mean an inherited break. About 15 in 100 colon tumors show MSI. Only about 3 of those 15 come from Lynch syndrome. In most of the rest, MLH1 itself has no typo: it has been silenced by chemical caps on the start of the gene. A blood test then shows whether the break was inherited.

A positive blood test is news for every parent, brother, sister and grown child, each with a one-in-two chance of carrying the same broken copy. Testing them one by one is called cascade testing. A ten-minute call this week might reach a forty-year-old brother who has never had a colonoscopy. A relative who tests negative keeps the usual schedule: screening starts at forty-five. A carrier starts colonoscopies in their twenties or early thirties, depending on the gene. After that, a colonoscopy comes every year or two. Each one looks for growths while they are small enough to remove, before they can turn into cancer.

Aspirin helps too. In the CAPP2 trial, 861 carriers were assigned by chance to take aspirin or a placebo for at least two years. The aspirin dose was 600 milligrams a day, far above the low-dose pill some adults already take each morning for the heart. Follow-up ran about ten years. By then, 40 of the 427 on aspirin had colon cancer. On placebo, 58 of the 434 did. Aspirin meant about a third fewer cancers. It can also cause bleeding, so the dose is a question for a doctor.

The typos even turn against the tumor. A tumor with a broken inspector carries far more wrong letters. Researchers counted an average of 1,782 per tumor, against 73 in tumors whose inspector worked. A wrong letter, such as a C where a T belonged, can make a protein with a wrong piece, and immune cells can spot the wrong pieces. A tumor can hold those cells back through a protein on them called PD-1, which works like a brake. Drugs that release that brake shrank 4 of 10 colon tumors with a broken inspector. They shrank none of 18 tumors whose inspector worked.

In 2022, twelve people with rectal cancer and a broken inspector took such a drug, dostarlimab. They had it every three weeks for six months. In all twelve, the tumor was gone on every scan, scope and biopsy. None needed radiation, chemotherapy or surgery in the 6 to 25 months that followed.

At the sideline, a second imp has been waiting the whole time with an empty thread. It is not an inspector. It copies.

A Closing Invitation. Mr. DNA’s frog stood for any wrong letter a cell reads as its own. The inspector that catches those letters can break, and the break runs in families.

1. Picture the clipboard. Before you get up, think of the family-history box on your last checkup form: a line for each relative, a line for each age. Which lines did you leave blank, or fill with a guess? Whose age at diagnosis have you never heard said out loud?
2. Find the broken inspector. This weekend, before your next checkup, call one relative and ask who had colon or uterine cancer, and at what age. Start with the one who always knows who married whom. Two names and two ages can move your first screening years earlier. Who else needs to hear the answers?
3. Ask what the tumor said. If a parent, brother or sister had colon or uterine cancer, ask this month whether the tumor was tested for the stutter or the repair proteins. An old pathology report may show “loss” beside a protein’s name. If the inspector was missing, who in the family has not been tested yet?

T always finds A because an imp walks every new strand and sets wrong letters right. In some families, that imp is broken. The phone that underlines your typos can find a broken one while T still finds A.

Worth remembering Save as image

Every cell runs a spellcheck on its DNA. When a family inherits a broken copy, one more break can switch it off, so cancer tends to come young. Ask your parents how old each relative was when cancer found them.

Where This Practice Came From

The stutter was found in May 1993, a month before Jurassic Park opened. Three teams reported colon tumors whose repeat runs had changed length. Within a year, the broken genes had names: MSH2, then MLH1, human copies of repair genes first studied in bacteria. Paul Modrich worked out how that bacterial crew fixes mismatched pairs, and shared the 2015 Nobel Prize in Chemistry for it. Watson and Crick’s 1953 paper had seen the copying coming: “It has not escaped our notice that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material.”

Intellectual Honesty Note. The sprites, the imps, the football field, the smell and the snap are invented staging; the Narrator names the real mechanism. Real mismatch repair cuts out a stretch of the new strand and copies it again, not one bead. The field holds one copy of the genome; a real cell holds two, one from each parent. Predictive text, the red squiggle and “nooooo” are this piece’s images, not biologists’ terms. The three-relatives rule is a short form of the clinical checklist, which also asks for close relatives and counts other Lynch cancers. The aspirin trial’s one-third is its hazard ratio of 0.65, and its likely range, 0.43 to 0.97, runs from a large benefit to almost none. The PD-1 study and the dostarlimab trial were small, and the second still needs longer follow-up. The film’s frog is its own science: only a few frog species have been reported to change sex.

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Near the edge of the frame, a few cells hang straight down, long and bumpy, like peanut shells made of wax (Figure 1). In each one, a larva floats on a pool of thick white jelly, far more than it can eat.

Figure 1. Two queen cells on the comb, one turn of a loop. A larva fed royal jelly in each will come out a queen, and the queen will lay the eggs of the workers who feed the next one. Photograph by Piscisgate (2014), Wikimedia Commons, CC BY-SA 4.0.

Any female larva in the hive can grow into a queen or a worker. Her genes do not decide which. The larvae in the hanging cells become queens. A queen lives for years and can lay more than a thousand eggs a day. A worker lives a few weeks in summer and usually lays none.

Food decides which. The white jelly is royal jelly (Figure 2), a rich food made in glands in the workers’ heads. The workers feed it to a few larvae for as long as they are larvae. The rest get a plainer mix with pollen and honey in it, and become workers. Food cannot rewrite a gene. So what does it change?

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Figure 2. How royal jelly makes a queen, from SciShow (2015), YouTube embed. The video credits one jelly protein, royalactin. A later team could not reproduce that result.

Think of a larva’s genes as a cookbook. Each gene is a recipe for one molecule the body uses, and every larva in the hive carries the same book. Cells can stick small chemical marks onto some of the recipes, like notes in the margin that say “skip this one.” Biologists call them methylation marks. They help decide which recipes the cell cooks and which it skips.

In 2008, a team at the Australian National University, in Canberra, tested whether those notes were what the jelly changed. The team switched off one gene in newly hatched larvae: the recipe for the enzyme that writes the notes. Then they fed the larvae a worker’s diet. Most of them came out as queens, with full ovaries. The team called the result “a royal jelly-like effect.” Each larva kept the cookbook it was born with. What changed was which recipes got cooked.

Which bee each larva became depended on what its cookbook was connected to: the notes, the food, and the workers who chose which larvae to feed. Any cookbook raises five questions: what it counts, what it keeps, what it answers, what it misses, and what it cannot decide.

Say you mail a spit sample to a DNA testing company, and the report comes back: you probably cannot digest milk as an adult. You start drinking your coffee black, bitter at the first sip. You stop buying cheese, pay extra for lactose-free milk and read every label in the shop. Your partner switches to oat milk so the fridge needs only one carton. By your next checkup, you have gone months without an easy source of calcium.

Here is how such a report could be wrong. For most people in the world, the body puts the recipe for digesting milk away after childhood. Some people carry a one-letter difference in the cookbook that keeps the recipe in use. In Europe, most people who have one share the same spelling. Many families who kept cattle in East Africa carry a different spelling that keeps the same recipe in use. Say the test looks only for the European spelling. A person who carries the East African one gets a report that finds nothing it knows and says the recipe is closed. That person gave up milk for nothing. The test read the right page, looked for the wrong spelling, and never asked where the family came from. Systems thinking has a question for any test result that costs someone milk, cheese and calcium: what else is that result connected to?

What the Cookbook Counts

Counting human genes started as a bet. In May 2000, at Cold Spring Harbor, the geneticist Ewan Birney opened a pool on how many genes human DNA would turn out to hold. Biology was about to get its first full cookbook for a person: every gene, every recipe (Figure 3).

Figure 3. The human genome printed as books at the Wellcome Collection, in London: a volume or more for each chromosome, from 1 to 22, then X and Y, in type almost too small to read. Photograph by Russ London (2010), Wikimedia Commons, CC BY-SA 3.0.

The guesses ran from about 20,000 to more than 200,000. In 2003, the count came in at 24,847. The closest guess, 25,947, belonged to Lee Rowen, who worked at the Institute for Systems Biology. She won $600 and a signed copy of The Double Helix.

Later counts settled lower, near 20,000. The worm C. elegans, about a millimeter long, has a little over 20,000 genes of its own. A person and a worm carry cookbooks of about the same size, so the number of recipes could not be what makes a person a person. In Donella Meadows’ definition of a system, the parts matter less than the rules that connect them. Here the parts are the genes, and the rules decide which recipes get cooked, when, and how much. Two kitchens with the same book can serve very different dinners.

A full gene count is one example of omics: measuring one layer of a living thing all at once. Each layer takes the suffix -ome. Two of them explain the bees.

In this piece’s kitchen, the genome is the cookbook, and the epigenome is the notes in its margins. The genome is the layer the walkthrough of DNA, transcription, and translation takes apart. The epigenome is the layer the natural experiment on methylation follows.

The book also closes some recipes on its own schedule, and a single letter can keep one open for life.

What the Cookbook Keeps

Milk is the recipe most bodies put away. Babies make their own enzyme for lactose, the sugar in milk. The enzyme is called lactase, and in most mammals the body stops making it after weaning. A short stretch of DNA near the gene closes the recipe after childhood. In about a third of adults alive today, the recipe stays open. The European spelling is a single changed letter in that stretch, and it keeps lactase coming for life.

The East African spellings are other one-letter differences nearby, and each arose on its own. In 2007, the geneticist Sarah Tishkoff and her colleagues traced the most common of them, carried by many herding peoples in Kenya and Tanzania. It had spread fast, over roughly the last seven thousand years.

Why keep that page open? Herds. Herds put fresh milk within reach. Adults who carried the spelling could digest the milk, got more food from it, and more of their children lived to carry the spelling too. The more people could drink milk, the more a herd was worth, and herding spread further. In Meadows’ terms for feedback, that is a reinforcing loop: a change that feeds itself. Even this loop has a ceiling. A herd can grow only as large as the grass and water around it allow. The cookbook kept the page. The herds outside made it worth keeping.

A DNA sample can show which spelling someone carries. It cannot show the herds that made the spelling worth carrying, or the grass and water that capped the herds. So a kit report that rules out milk earns one email to the company within the week: which spellings did the test look for? A parent who skips the email may cut milk from the children’s plates too, on a test that never looked for the spelling the family carries. A parent who already cut the milk can still ask.

What the Cookbook Answers

The herds and their milk changed the book over thousands of years. The body asks the book questions every day, and it answers within hours.

In 2012, Romain Barrès and his colleagues put eight sedentary men on an exercise bike twice, at least a week apart. One ride was easy, at 40 percent of each man’s maximum effort, and one was hard, at 80 percent. Both rides stopped once the rider had burned 400 calories. With a needle, the researchers took small plugs of thigh muscle before each ride, right after it, and three hours later.

One recipe they read was PGC-1α, which tells a cell to build more of its energy supply. Right after the hard ride, the notes on PGC-1α had dropped to about half their resting level. Three hours later, the muscle was cooking that recipe several times as much as at rest. After the easy ride, the notes barely moved, yet the recipe still got cooked more. The notes are one rule among several.

That energy supply is mitochondria (Figure 4), the parts of a cell that burn fuel. Over months of training, more mitochondria mean more capacity for the next ride.

The ride changes the notes. The notes change which recipes get copied out to the counter, a layer called the transcriptome. The copies change which dishes get made, the proteome. The dishes change what the body can do on the next ride. The cookbook answers the ride, and the answer shapes the next question.

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Figure 4. What more mitochondria do for a cyclist, from Pedaling to the Top (2025), YouTube embed. Thumbnail: two mitochondria in lung tissue, electron micrograph by Louisa Howard, public domain.

To see the answer, the team had to sample the muscle three times in one day. Many omics studies draw one tube of blood from each person, once. Peter Senge defines systems thinking as seeing “patterns of change rather than static ‘snapshots.’” One tube is a snapshot. It can show the notes in the margins, but not which ride wrote them.

What the Cookbook Misses

Reading 5.4 million genomes still left out the meals. In 2022, a study led by the geneticist Loïc Yengo pooled those genomes. It found 12,111 small spellings tied to height, each with a tiny effect. Together, in people of European ancestry, they account for about 40 percent of how much heights differ. In other ancestries, the share falls to about 10 to 20 percent. Part of the 60 percent the spellings miss is genetic and not yet mapped.

The rest sits on the plate. In the 1800s, Dutch soldiers averaged about 165 centimeters, shorter than men in most of Europe. Dutch men are now the tallest in the world. They stand about 20 centimeters taller, most of a head above those soldiers. A cookbook cannot change that fast. Food, health, and living conditions can.

Say a youth basketball coach ranks twelve-year-olds by a height score built from those 12,111 spellings and cuts the bottom three. A parent shown the ranking can ask which people the score was built on. The score says less for players outside the ancestry it was built on, and nothing about what their childhood meals will add.

What the Cookbook Cannot Decide

A cell can hold a recipe and still never cook it.

Malaria kills close to 600,000 people a year, most of them young children in Africa. One of the main malaria drugs is artemisinin (Figure 5), which comes from a plant called sweet wormwood. The supply of wormwood swings. A short harvest sends the price up, so more farmers plant wormwood. Once their crops flood the market, the price falls, and the next shortage begins.

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Figure 5. A short history of malaria drugs, from NPR’s Skunk Bear (2012), YouTube embed.

In 2003, a team led by the chemical engineer Jay Keasling, at Berkeley, looked for a steadier source. They copied recipes from baker’s yeast and one from wormwood into E. coli, and the bacteria made an early form of the drug. The team then moved the work into yeast itself. In April 2013, the drug company Sanofi started making artemisinin with yeast in Garessio, in northern Italy. That year, the factory made about 8 percent of the world’s supply.

By 2015, farmers had a great year. So much wormwood grew that artemisinin from the plants sold for less than $250 a kilogram. Sanofi needed $350 to $400 to break even. That is at least $100 a kilogram above the plants. Sanofi’s rivals would not buy from it, and the world wanted no more of the drug than before.

“If that price is already very low and there’s a bumper crop,” Keasling said, “there’s no reason to fire up a fermenter.” The fermenter, the steel tank where the yeast grows, stood idle. The yeast still had the recipe. The price of wormwood decided.

That is the edge of every cookbook. No page inside the yeast held the price of wormwood. The jelly, the herds, the ride, the meals and the market all came from outside the book, and each one decided what got cooked.

A test report that says to give up a daily food has read one book. A friend holding such a report can ask three things first. What did the test look for? Which people was it built on? What else is the result connected to? The larva’s cookbook could not say which bee it would become. The jelly in its cell could.

A Closing Reflection. The cookbook counted, kept, answered and missed, and it did not decide. The jelly, the herds, the ride, the plate and the price of wormwood each changed which recipes reached the table, and none rewrote a recipe.

1. Spot the idle fermenter. Right now, look around for something you paid for that still works and stands unused: a bread maker in the cupboard, an app on the phone in your hand. It still has its recipe. What around it changed?
2. Read the margin notes. Think back to one habit that changed this year. Something around you changed first: a new gym on your street, an office move that added forty minutes to the commute, a friend who started walking at six. Which of your own recipes got cooked more, which got skipped, and who at home noticed first?
3. Ask which spelling. When the next report tells you to give up a food, from a DNA kit or your next checkup, ask what the test looked for before the shopping changes. One question may keep the cheese on the table. Who would give the food up with you, the one who cooks or the one who shops?

Open a packet of baker’s yeast and smell it. Split the dough: one bowl by a warm window, one in a cool corner. Look again in an hour. Same packet, same recipe. One bowl rose like a queen.

Worth remembering Save as image

You can read every page of the cookbook and still not know what is for dinner. Your genes hold the recipes; what gets cooked is decided outside the book.

Where This Came From

This piece follows systems thinking into a single cell. Konopka’s post on systems thinking (2026) started it.

Intellectual Honesty Note. The cookbook is this piece’s image, not a biologist’s term: genes as recipes, methylation marks as notes in the margin, gene variants as spellings, RNA copies as recipes copied out, proteins as dishes. A methylation mark does not always mean “skip”; on the genes in the exercise study, fewer marks went with more activity. The hive scene is built from standard beekeeping descriptions, not one hive.

The stakes paragraph’s report is hypothetical, and which spellings a kit tests depends on the kit. This piece reads lactase persistence as a reinforcing loop with a grazing ceiling. It adds the exercise loop’s last step, “more capacity for the next ride.” Its point about a snapshot not naming the ride is its own reading, not a finding. The stretch of DNA near the lactase gene is an enhancer, which raises a gene’s activity; “closes the recipe” simplifies how it is turned down. The exercise study measured single rides, not months of training. The 60 percent and the $100 gap are subtractions made here from the cited numbers, and the ride’s “about half” and “several times” are read off the exercise paper’s Figure 2. The protein step and the link from PGC-1α to mitochondria are standard physiology. The bee experiment switched the methylation enzyme off by hand; how much methylation steers caste in an ordinary hive is still debated (Oldroyd and Yagound, 2021).

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