The short answer
Yes. Humans are still evolving, and we can name the genes.
The question usually comes from a reasonable place. Modern medicine saves people who would once have died young. Farming means food is not a constant struggle for most of the world. It feels like the harsh filter has been switched off.
It has not been switched off. It has been swapped for a different one.
What “still evolving” actually means
Evolution is a change in how common inherited variants are in a population over generations. It is not about individuals improving. A person does not evolve. A population does.
So the test is simple. Can we find variants in human DNA that have clearly become more or less common in the recent past, for reasons we can identify? We can. Here are four cases.
Milk: the most famous recent example
Nearly all mammals stop producing the enzyme lactase after weaning. There is no point making an enzyme for milk sugar once you no longer drink milk. Most adult humans on Earth follow the same pattern and lose the ability too.
But some populations keep lactase switched on for life. Scientists call this lactase persistence.
In Europeans, the key change is a single DNA letter about 13,910 positions upstream of the lactase gene. It acts like a switch stuck in the on position.
Then comes the interesting part. Sarah Tishkoff and colleagues studied 470 people from Tanzania, Kenya, and Sudan, and published the results in the journal Nature Genetics. Many of those people could digest milk as adults. Almost none of them carried the European change.
Instead they carried three different changes, at nearby but separate positions, sitting on completely different stretches of surrounding DNA. Different mutations. Same result.
The team estimated that the main African variant spread within roughly the last few thousand years, somewhere around 3,000 to 7,000. That matches the archaeology. Cattle herding spread into East Africa around 4,500 years ago.
This is convergent evolution in our own species, within recorded human history. And the pressure that drove it was not climate or predators. It was a human invention. People started keeping animals for milk, and the gene followed the culture.
Thin air: two different solutions
The Tibetan Plateau sits around 4,000 metres above sea level. The air there holds far less oxygen than air at the coast. A visitor from sea level gets breathless, sleeps badly, and can become seriously ill.
The usual short-term response is to make more red blood cells. That carries more oxygen, but it also thickens the blood, which strains the heart and causes problems in pregnancy.
Tibetans do not do this. They live at altitude with hemoglobin levels much closer to a sea-level person’s, and they manage fine. A gene called EPAS1, part of the body’s oxygen-sensing pathway, carries the strongest signal of selection found anywhere in the Tibetan genome.
In 2014, Emilia Huerta-Sanchez and colleagues re-sequenced the EPAS1 region in 40 Tibetan and 40 Han Chinese individuals. The Tibetan version had a strange structure that ordinary mutation could not easily explain. It matched Denisovan DNA.
Read that again. A gene variant that helps people live on the Tibetan Plateau today was inherited from a different human group that died out tens of thousands of years ago. Interbreeding with Denisovans handed our ancestors a piece of useful equipment.
Now compare the Andes. Andean populations have also lived at extreme altitude for thousands of years, and they are also well adapted. But they solved it differently. Cynthia Beall’s work shows that Andean highlanders do raise their hemoglobin concentration, while Tibetans instead breathe more and keep hemoglobin low.
Two populations. Same problem. Two different biological answers. Evolution does not search for the best solution. It works with whatever variation happens to be present.
Malaria and sickle cell: a real trade, with a real cost
This is the clearest case of evolution having no kindness and no goal.
A single DNA letter change in the beta-globin gene produces a slightly different hemoglobin molecule, called HbS.
If you inherit two copies, you have sickle cell disease. Red blood cells deform into stiff crescents, block small vessels, and cause pain crises, organ damage, and anemia. It is a serious illness.
If you inherit one copy, you have sickle cell trait, and you are strongly protected against severe malaria. Studies reviewed in Malaria Journal in 2013 put that protection in the range of 70 to 90 percent against severe malaria, with even higher figures reported for cerebral malaria in some studies.
So the variant carries a heavy cost and a large benefit, and which one dominates depends entirely on where you live. In regions where falciparum malaria is common, the variant stays at high frequency. Where malaria is absent, it stays rare.
Natural selection is not looking after anyone’s health. It keeps whatever leaves more descendants on average across a population. Sometimes that average hides real suffering.
CCR5-delta32: an honest complication
CCR5 is a protein that sits on the surface of certain white blood cells, like a door handle. The most common form of HIV grabs that handle to get inside the cell.
Some people carry a version of the gene called delta32, which is missing 32 DNA letters. In them, the handle never gets built. People with two copies are highly resistant to infection by the common form of HIV. Across Europe the variant sits at roughly 5 to 14 percent of copies. It is most common in the north and rarer further south.
Here is the honest part. For years, many researchers assumed some past epidemic, perhaps plague or smallpox, had pushed this variant up in frequency. An early estimate even placed its origin around 700 years ago, which fitted the plague story neatly.
Then in 2005, Pardis Sabeti and colleagues re-examined it in the journal PLOS Biology. Their paper was titled “The Case for Selection at CCR5-delta32”, and its conclusion went against the popular story. Using better genetic maps, they found the variant is probably more than 5,000 years old, far too old for a medieval epidemic to explain. They also found that the pattern of DNA around the gene does not stand out from the rest of the genome. It looks like ordinary chance, not unusually strong selection.
The argument is not fully settled, and the authors did not rule selection out. But two things are clear. HIV is far too recent to have shaped how common delta32 is. And a variant can be extremely useful today without ever having been favoured for that use.
That is worth remembering whenever anyone describes a gene as being “for” something.
”Medicine stopped evolution” and why it is wrong
The claim sounds sensible and falls apart quickly.
First, evolution needs variation and unequal reproduction. It does not need disease. As long as some people have more children than others, and any of the difference is inherited, gene frequencies shift.
Second, medicine changes which pressures matter rather than removing pressure. Before antibiotics, resistance to certain infections was a matter of life and death. Now other things matter more. The filter changed shape. It did not disappear.
Third, natural selection is only one of several mechanisms. Mutation keeps producing new variation. Every baby is born carrying roughly 50 to 70 new mutations that neither parent had. Genetic drift shifts frequencies by chance alone, especially in small populations. Migration moves variants between groups. None of these care about hospitals.
Fourth, evolution is slow at the scale of a human life. Lactase persistence took thousands of years. Expecting to see visible change over one century is like expecting to watch a glacier move by staring at it.
Culture and migration now shape our gene pool
Two forces are unusually strong in humans right now.
One is culture. The milk example shows it plainly. A cultural invention, dairy farming, created a biological pressure that rewrote a gene’s frequency across whole continents. Cooking, farming, cities, and clothing all did something similar to earlier populations.
The other is movement. For most of history, people had children with people born nearby. Today, populations that were separated for tens of thousands of years mix within a single generation. In evolutionary terms this is gene flow, and it is running faster than at any earlier point in human history. It generally reduces differences between populations rather than increasing them.
There is also sheer scale. With around 8 billion people alive, more new mutations arise in the human population every generation than ever before. Most do nothing. A few will matter.
What this does not mean
It does not mean humans are becoming smarter, stronger, or better. Evolution has no direction and no destination.
It does not mean any human population is more evolved than another. Every living population has exactly the same amount of evolutionary history behind it.
It does not mean you can watch it happen in your lifetime. The changes described above took hundreds of generations.
What it does mean is simple. We are not finished, and we were never outside the process.
Where to go next
To see how the mechanism works step by step, read natural selection. For more cases measured directly by scientists, read observed evolution. To see where the raw variation comes from in the first place, read mutation.