Seborrheic keratoses are caused by an overgrowth of ordinary skin cells, driven by a combination of genetic mutations that accumulate over a lifetime, sun exposure, and aging. They are completely benign, and nearly 100 percent of people over 60 have at least one. Despite how common they are, the exact trigger that starts any individual growth remains partly unclear, though research has identified several key contributing factors.
Somatic Mutations in Skin Cells
The most well-understood cause is a set of acquired mutations, meaning changes in DNA that happen during your lifetime rather than ones you’re born with. These mutations occur in the genes that control how skin cells grow and divide. In a study of 25 seborrheic keratosis lesions, 48 percent carried mutations in a gene called FGFR3, which acts as a growth signal for skin cells. Another 32 percent had mutations in PIK3CA, a gene involved in cell survival and proliferation. About a quarter of lesions showed mutations in the gene that controls telomerase, an enzyme that lets cells keep dividing beyond their normal lifespan.
What’s notable is that these are the same kinds of mutations found in some cancers, yet seborrheic keratoses never become malignant. The mutations push skin cells to multiply more than usual, creating a raised, thickened patch, but something keeps them biologically constrained. The growth stacks up layers of skin cells on the surface, which is why the lesions often have that characteristic waxy, “stuck-on” appearance.
Cumulative Sun Exposure
UV radiation plays a significant role, though it’s not the whole story. Genome-wide sequencing of seborrheic keratoses has revealed a prominent UV-associated mutational signature, especially in lesions on chronically sun-exposed skin like the face, neck, and hands. This fits a model where decades of sun exposure gradually cause DNA changes in skin cells, and some of those changes eventually produce a seborrheic keratosis.
Animal research has added more detail to this picture. In mice genetically predisposed to reduced levels of a tumor-suppressing protein called PTEN, long-term UVA exposure (the type of UV that penetrates deeper into skin and passes through windows) caused growths resembling seborrheic keratoses. Mice without that genetic predisposition didn’t develop growths from the same UV exposure, which suggests that sun damage alone isn’t sufficient. It needs to interact with other vulnerabilities in the skin cell’s DNA.
That said, seborrheic keratoses also appear on skin that rarely sees the sun, like the back, chest, and under clothing. So while UV exposure accelerates the process, it’s clearly not the only path to developing these growths.
Aging
Age is the single strongest predictor. Seborrheic keratoses are rare in people under 30 and become progressively more common from middle age onward, reaching near-universal prevalence after 60. This makes sense given what we know about the mutations involved: the longer your skin cells have been dividing and accumulating small DNA errors, the more likely one of those errors will land in a growth-related gene. It’s essentially a numbers game played out over decades.
Older individuals are also more likely to have lesions with telomerase-related mutations, particularly on the head and neck, areas with the longest cumulative sun exposure. This overlap between aging and UV damage makes it difficult to tease the two apart, and both likely contribute simultaneously.
Family Tendency and Genetics
Seborrheic keratoses tend to run in families. If your parents developed many of them, you’re more likely to as well. The pattern suggests a genetic component to susceptibility, though no single inherited gene has been identified as responsible. What’s probably inherited isn’t the keratosis itself but a predisposition: skin that’s more likely to accumulate the specific mutations that lead to these growths, or less efficient at repairing the kind of DNA damage that triggers them.
Hormonal Changes
Some people develop new seborrheic keratoses during pregnancy or while taking estrogen replacement therapy. The American Academy of Dermatology notes this association, though the mechanism isn’t fully understood. Estrogen influences skin cell growth and turnover, so elevated hormone levels may accelerate the development of growths in skin cells that already carry some of the predisposing mutations. Hormonal shifts don’t cause seborrheic keratoses on their own, but they can act as a trigger in people who are already prone to them.
What About HPV?
For years, researchers investigated whether human papillomavirus (HPV) might cause seborrheic keratoses, since HPV is known to drive other skin growths like warts. The current consensus is that HPV is not a meaningful cause. Some studies have detected HPV DNA in seborrheic keratosis tissue, particularly in genital lesions, but this appears to be coincidental rather than causal. The etiology is still formally described as “uncertain” in medical literature, but the weight of evidence points firmly toward somatic mutations and UV exposure rather than viral infection.
When Rapid Growth Signals Something Else
In rare cases, a sudden eruption of many seborrheic keratoses over a short period, typically within a year, can be a sign of an internal cancer. This is called the Leser-Trélat sign. Unlike ordinary seborrheic keratoses that develop gradually over years, these appear rapidly, often look similar to each other, and show up in someone who previously had few or no such growths.
There are no standardized diagnostic criteria for the Leser-Trélat sign, but clinicians look for a temporal relationship: the skin lesions and the cancer appearing around the same time, the lesions worsening if the cancer progresses, and improving if the cancer is treated. This is a paraneoplastic phenomenon, meaning the cancer produces growth factors or other signals that stimulate skin cell proliferation throughout the body. It’s genuinely rare, and the vast majority of people developing seborrheic keratoses are experiencing the normal, age-related process described above.