Last reviewed: May 12, 2026 Last updated: May 12, 2026

Written by: Jay Hastings , CEO of PlexusDx

Jay Hastings is the CEO of PlexusDx, a precision health company focused on genetic testing, blood biomarker insights, and personalized wellness recommendations. He has more than 20 years of experience across healthcare innovation, genomics, laboratory operations, healthcare investing, and strategic finance. His work has included scaling healthcare startups, leading CLIA lab integrations, and helping expand consumer access to precision health tools.

Medically reviewed by: Jayden Lee, PharmD, EMBA

Jayden Lee, PharmD, EMBA, is the PlexusDx Medical Science Liaison with a PharmD and MBA specializing in pharmacogenomics and clinical product development, with a proven ability to bridge the gap between genomic research and practical patient outcomes. Dr. Lee has more than 10 years of professional experience in clinical pharmacy, academia, and research.

This article is part of the PlexusDx Education Hub — your resource for evidence-based guidance on Skin Health & Genetics. Browse all Skin Health & Genetics education

Actinic keratoses are rough, scaly patches that form on skin after years of sun exposure. They matter because they are precancerous: a small percentage can progress to squamous cell carcinoma if left untreated. Understanding what drives them — ultraviolet damage layered on top of inherited skin traits — is the first step toward protecting your skin.

What actinic keratosis looks like

Actinic keratoses typically appear on the most sun-exposed areas: the face, scalp, ears, neck, forearms, and backs of the hands. They can feel like sandpaper before they are easy to see, and may present as dry, scaly patches or raised, wart-like bumps. Some itch, burn, bleed, or crust over. Because they can resemble other skin changes, any new or persistent lesion deserves a professional look.

How UV damage drives it

Ultraviolet radiation is the primary cause. Over years, UV light damages the DNA of skin cells, and a recurring target is the TP53 gene — the so-called guardian of the genome. TP53 normally halts damaged cells from dividing; when UV mutations disable it, abnormal cells accumulate, which is the biological hallmark of actinic keratosis and its progression toward squamous cell carcinoma. This is why cumulative lifetime sun exposure, not a single burn, is the key risk.

Skin-type genetics and MC1R

Not everyone burns equally, and genetics explains much of the difference. The MC1R gene controls the balance of melanin pigments. Certain MC1R variants produce more red-toned pheomelanin and less protective eumelanin, giving fair skin, red or light hair, and a tendency to freckle and burn rather than tan. People with these variants accumulate UV damage faster, which raises susceptibility to actinic keratoses — a clear example of how an inherited gene shapes a sun-driven condition. Age and immune status compound this: most lesions appear after 40, when decades of exposure have added up, and people on immune-suppressing medication face higher risk because their skin polices abnormal cells less effectively.

Sun-protection strategies that work

Prevention is straightforward and effective: limit direct sun during peak hours (roughly 10 a.m. to 4 p.m.), apply broad-spectrum SPF 30 or higher and reapply it, wear hats and protective clothing, avoid tanning beds entirely, and check your skin regularly for new or changing spots. These habits reduce the cumulative UV dose that drives the underlying DNA damage.

When to see a provider

If you notice a persistent rough patch or a lesion that itches, bleeds, or will not heal, see a healthcare provider or dermatologist for evaluation. Clinicians have several established options — including cryotherapy, topical treatments, photodynamic therapy, and curettage — chosen based on the lesion. Early professional attention is how actinic keratoses are kept from progressing.

Understanding your genetic risk factors

Your skin-type genetics set your baseline UV sensitivity, but daily sun behavior determines how that risk plays out. The PlexusDx Precision Peptide Genetic Test examines 14 pathways, 49 peptides, 150+ genetic insights, offering pathway-level context about traits such as UV response rather than a skin-cancer diagnosis. PlexusDx tells you about your biology; it does not tell you what to put in your body. Screening and treatment stay with a qualified clinician.

Frequently Asked Questions

Is actinic keratosis skin cancer?

Actinic keratosis is precancerous, not cancer itself. A portion of untreated lesions can progress to squamous cell carcinoma over time, which is why early detection matters. A healthcare provider can determine whether a lesion needs treatment or monitoring based on its appearance and your risk factors.

Which genes influence actinic keratosis risk?

MC1R variants that produce fair skin and a tendency to burn raise susceptibility by allowing faster UV damage. UV-induced mutations in the TP53 gene are a hallmark of the lesions themselves. Together they show how inherited traits and sun exposure combine to drive the condition.

How can I prevent actinic keratoses?

Reduce cumulative UV exposure: use broad-spectrum SPF 30 or higher, seek shade during peak hours, wear protective clothing and hats, and avoid tanning beds. Regular skin self-checks help you catch changes early. These steps lower the DNA damage that underlies actinic keratosis development.

Does the PlexusDx test detect skin cancer?

No. The Precision Peptide Genetic Test provides pathway-level educational insight into traits like UV sensitivity. It does not diagnose, treat, or prevent actinic keratosis or skin cancer. Any suspicious skin lesion should be evaluated by a dermatologist or qualified healthcare provider.

Curious how your genetics may shape UV-response and related pathways? Explore the PlexusDx Precision Peptide Genetic Test.

This article is part of the PlexusDx Education Hub. Browse all Skin Health & Genetics education

The Precision Peptide Genetic Test analyzes how your genes influence peptide-related biological pathways. It does not recommend, prescribe, or determine which peptides you should use. Consult a qualified healthcare provider before beginning any peptide protocol.

Medical and Editorial Standards

Medical review process: This article was reviewed for medical accuracy, scientific clarity, evidence alignment, and appropriate discussion of genetics, medications, supplements, biomarkers, and health-related claims.

Sources and evidence: PlexusDx educational content is developed using peer-reviewed research, clinical literature, reputable medical references, and, where applicable, public health or regulatory guidance. References are included at the end of the article when scientific, medical, or health-related claims are discussed.

Commercial transparency: PlexusDx offers genetic testing, blood biomarker testing, personalized supplement recommendations, and related precision wellness services. Product mentions are intended to help readers understand available options and should not be interpreted as medical advice.

Important disclaimer: PlexusDx educational content is for informational purposes only and should not be used as a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider before making decisions about medications, supplements, genetic testing, lab testing, or health-related care.