Seborrheic keratoses are caused by the overgrowth of ordinary skin cells called keratinocytes. These cells begin multiplying in a controlled but excessive way, forming the waxy, stuck-on bumps that are among the most common benign skin growths in adults. Over 90% of people older than 60 have at least one. The underlying triggers involve a combination of genetic mutations, cumulative sun exposure, aging, and possibly hormonal influences.
How These Growths Form at the Cellular Level
A seborrheic keratosis starts when a small group of skin cells in the outer layer of skin begins dividing more than it should. This is called clonal expansion: a single cell picks up a mutation that tells it to keep growing, and its descendants form a visible bump. The growth stays benign because, unlike cancer, these cells don’t invade deeper tissue or spread to other parts of the body. They just pile up, creating the characteristic raised, rough, or waxy appearance.
As the cells accumulate, the outer layer of skin thickens. Depending on the particular growth pattern, you might see heavy surface scaling, a deeply pigmented bump, or tiny cyst-like structures embedded in the lesion. These variations explain why seborrheic keratoses can look so different from one another, ranging from flat tan patches to dark, rough, almost wart-like bumps.
Genetic Mutations That Drive Growth
The single most important molecular driver is a mutation in a gene called FGFR3, which encodes a receptor on the cell surface that normally helps regulate cell growth. When this gene is stuck in the “on” position, it continuously signals the cell to divide. Activating mutations in FGFR3 have been found in roughly 85% of one common subtype of seborrheic keratosis.
A second frequently mutated gene, PIK3CA, works through a related growth-signaling pathway. Together, FGFR3 and PIK3CA mutations push cells down a path of sustained but non-cancerous proliferation. Additional mutations in gene promoters that control an enzyme involved in cell lifespan (telomerase) have been identified in a subset of lesions, particularly those on the head and neck of older individuals. These mutations may help the abnormal cells survive longer than they normally would.
Importantly, genome-wide sequencing of seborrheic keratoses has revealed a strong ultraviolet radiation signature in the DNA, especially in lesions from chronically sun-exposed skin. This means the mutations driving these growths are often the direct result of accumulated sun damage over a lifetime, not random copying errors.
The Role of Sun Exposure
Cumulative UV exposure is considered a major risk factor. The connection shows up in several ways: the mutations found in seborrheic keratoses carry the hallmark fingerprint of UV-induced DNA damage, lesions are most common on sun-exposed areas like the face, neck, chest, shoulders, and back, and the number and size of growths increase with age, which correlates with more total sun exposure over time.
That said, the relationship isn’t perfectly straightforward. Studies measuring current sun exposure levels have not always found a direct correlation with lesion size at any given moment. One study in a coastal population found no significant difference in lesion diameter between people with high versus low sun exposure indexes. This suggests that it’s the cumulative, decades-long UV damage to skin cell DNA that matters, not recent sun habits. UV radiation also increases the production of a protein associated with skin aging and damage, which may further accelerate seborrheic keratosis development.
Aging Is the Strongest Risk Factor
Age and seborrheic keratoses go hand in hand. These growths are rare in children and uncommon before age 30, but they become nearly universal in older adults. By age 60, an estimated 9 out of 10 people have at least one. Both the number and size of lesions tend to increase with each passing decade.
This isn’t just about more years of sun exposure. Aging skin accumulates more mutations in general, the cellular repair machinery becomes less efficient, and growth-regulating pathways may become less tightly controlled. The promoter mutations in the telomerase gene, which appear more often in older people’s lesions, hint that age-related changes in how cells manage their own lifespan play a direct role.
Hormonal and Growth Factor Influences
Hormones may also play a part, though the evidence is less definitive than for UV exposure or genetics. Seborrheic keratoses have been observed to change in behavior during pregnancy or in people taking sex steroid hormones like estrogen. Research has found that the concentration of epidermal growth factor receptors (proteins on the cell surface that respond to growth signals) is notably elevated in actively growing seborrheic keratoses, particularly in people who are pregnant or using hormone therapy.
This suggests that sex hormones can amplify the growth signals that drive these lesions, potentially explaining why some people notice new or enlarging growths during hormonal shifts. However, hormones alone don’t cause seborrheic keratoses. They appear to act more like an accelerator when the underlying genetic mutations are already present.
Where They Tend to Appear
Seborrheic keratoses show up most often on the face, neck, chest, shoulders, and back. The back is an especially common site. Very small growths can also cluster around the eyes or elsewhere on the face, sometimes called flesh moles. These clustered lesions, known as dermatosis papulosa nigra, are particularly common in people with Black or brown skin. The palms of the hands and soles of the feet are typically spared.
The preference for the trunk and face aligns with the UV exposure theory, since these areas receive significant sun over a lifetime. But seborrheic keratoses can also appear in areas with less sun exposure, reinforcing the idea that UV light is an important contributor, not the sole cause.
When Sudden Eruptions Signal Something Else
In rare cases, a large number of seborrheic keratoses appear suddenly rather than gradually. This pattern, known as the Leser-Trélat sign, has been linked to underlying internal cancers, most commonly stomach, colon, and breast cancers, as well as lymphomas. The idea is that a growing tumor elsewhere in the body releases growth factors that trigger rapid development of skin lesions.
This association remains somewhat controversial in dermatology. There are no standardized diagnostic criteria for the Leser-Trélat sign, and many experts remain skeptical because the connection doesn’t consistently meet the formal benchmarks used to confirm a link between skin signs and internal cancers. Seborrheic keratoses are so common in older adults that coincidental timing with a cancer diagnosis is plausible. Still, a sudden eruption of many new growths, especially alongside other unexplained symptoms like weight loss or fatigue, is worth bringing to a doctor’s attention.
How Doctors Confirm the Diagnosis
Because seborrheic keratoses can sometimes mimic melanoma or other skin cancers visually, doctors often use a handheld magnifying tool called a dermatoscope to examine the surface in detail. Under magnification, seborrheic keratoses have distinctive features that set them apart from concerning lesions. The most common finding is comedo-like openings (tiny dark pore-like structures), present in about 68% of cases. Fissures and ridges, which look like cracks along the surface, appear in roughly 62%. Small white or yellow cyst-like dots, corresponding to tiny keratin-filled cysts within the growth, show up in about 38% of cases.
These features, along with a clearly defined border that looks almost stamped onto the skin, give doctors confidence in distinguishing a harmless seborrheic keratosis from something that needs a biopsy. When the visual features are ambiguous, a small tissue sample can confirm the diagnosis under a microscope.