Athlete's Foot Runs in Families? The Genes Behind Fungal Skin Infections

Every gym changing room has it. The fungus that causes athlete's foot lives on damp floors, in shared showers and inside trainers, and most people who use them walk across it every week. Some of them get itchy, peeling toes or a thickened, yellowing toenail. Many never do.

The usual explanation is luck and flip-flops. Those matter. But the largest genetic study of fungal skin infection has found that part of the difference is written in the skin itself — and in a gene that most people know for an entirely different reason.

One in five people

The fungi are called dermatophytes, and the infections they cause — athlete's foot, nail fungus, ringworm, the itchy rash in the groin — are grouped as dermatophytosis. Together they affect around 20% of the world's population.

Haapaniemi et al. 2026 combined the health records and DNA of four huge biobanks — FinnGen, the Estonian Biobank, UK Biobank and the Million Veteran Program — for over 250,000 people with a fungal skin infection and about 1.37 million without. They found 30 places in the genome where the risk changes, and when they looked at nail fungus and athlete's foot separately, 44 signals.

A wall made of keratin

The fungi feed on keratin, the tough protein of skin, nails and hair, so the first place to look is the wall itself. Several of the top signals sit beside genes that build it. One is near FLG, the gene for filaggrin, which helps hold the outer layer of skin together and is best known from eczema; another is near KRT77, a keratin gene. For athlete's foot on its own, one of the positions on this site, rs184587444, sits among the SPRR genes, a family that toughens the skin's surface.

The study also found genetic overlap with other skin conditions. A skin barrier that lets water out and irritants in seems to let fungi in too.

The guards at the gate

Another top signal is in HLA-DQB1, part of the system that shows the immune system what it is fighting. That fits a pattern the infection and immunity topic follows across many diseases: whether a microbe stays or goes is decided as much by the host as by the microbe.

The surprise: an obesity gene

Then there is FTO. It is the most famous obesity gene in genetics, and it is one of this study's top signals. Its position rs1421085 is filed on this site under obesity, and here it turns up again. The study also found genetic overlap with obesity-related traits and names obesity as one of the factors in fungal infection risk.

The paper does not say how the link works, and this page will not guess. What the genetics shows is that the same stretch of DNA that nudges body weight also nudges the odds of fungal infection.

Where this touches this site

19 of the study's positions already have pages here. Five are on the dermatophytosis page, and the strongest of those, rs7196726 near ZNF646, has an odds ratio of 1.07: a small shift, like nearly every common variant. Another, rs10094888, sits near SLURP2, one of the study's top genes. The Gene Knowledge Graph shows each of these genes with every condition it reaches.

So the flip-flops still help. But the next time a friend never seems to catch it while you always do, part of the answer may be in the wall of your skin, the guards at its gate, and a gene you thought was only about weight.