UV radiation is a major modifiable risk factor for skin cancer and other skin disorders. It is classified as a "complete carcinogen" due to its mutagenic and damaging properties, as well as its role in both tumor initiation and promotion. UV radiation also has beneficial effects, such as promoting vitamin D synthesis and endorphin production, but excessive exposure leads to skin damage, atrophy, pigmentation changes, and malignancy. UV is epidemiologically and molecularly linked to three common skin cancers: basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. Genetic factors, particularly polymorphisms in the melanocortin 1 receptor (MC1R) gene, influence UV-related skin disease risk. MC1R is crucial for melanin production and skin pigmentation, which determines UV sensitivity and cancer risk. The skin is composed of two layers, the epidermis and dermis, with the epidermis being the outermost layer. Keratinocytes, the most abundant cells in the epidermis, form a barrier and accumulate melanin, which blocks UV penetration. Melanocytes, which produce melanin, are found in the epidermis and dermis. Melanin comes in two forms: eumelanin, which is more effective at blocking UV, and pheomelanin, which is less effective and may promote oxidative DNA damage. Skin pigmentation is determined by melanin levels, with fair-skinned individuals having less eumelanin and thus higher UV sensitivity and cancer risk. UV radiation is divided into UVA, UVB, and UVC, with UVA penetrating deeper into the skin and UVB causing direct DNA damage. UV exposure varies geographically and is influenced by factors such as altitude, cloud cover, and latitude. Indoor tanning increases UV exposure and skin cancer risk, with significant increases in melanoma risk for those who tan before age 35. UV-induced DNA damage leads to mutations and cancer, with the NER pathway playing a critical role in DNA repair. Xeroderma Pigmentosum, a genetic disorder, results from NER deficiencies and leads to severe UV sensitivity and skin cancer. The melanocortin 1 receptor (MC1R) is a key gene involved in pigmentation, tanning, and skin cancer susceptibility. MC1R polymorphisms are associated with fair skin, sun sensitivity, and increased melanoma risk. MC1R signaling enhances melanin production and DNA repair, reducing UV-induced damage. Pharmacologic manipulation of cAMP levels may help reduce UV sensitivity and cancer risk. Overall, UV exposure is a major risk factor for skin cancer, and minimizing UV exposure is crucial for reducing skin cancer incidence.UV radiation is a major modifiable risk factor for skin cancer and other skin disorders. It is classified as a "complete carcinogen" due to its mutagenic and damaging properties, as well as its role in both tumor initiation and promotion. UV radiation also has beneficial effects, such as promoting vitamin D synthesis and endorphin production, but excessive exposure leads to skin damage, atrophy, pigmentation changes, and malignancy. UV is epidemiologically and molecularly linked to three common skin cancers: basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. Genetic factors, particularly polymorphisms in the melanocortin 1 receptor (MC1R) gene, influence UV-related skin disease risk. MC1R is crucial for melanin production and skin pigmentation, which determines UV sensitivity and cancer risk. The skin is composed of two layers, the epidermis and dermis, with the epidermis being the outermost layer. Keratinocytes, the most abundant cells in the epidermis, form a barrier and accumulate melanin, which blocks UV penetration. Melanocytes, which produce melanin, are found in the epidermis and dermis. Melanin comes in two forms: eumelanin, which is more effective at blocking UV, and pheomelanin, which is less effective and may promote oxidative DNA damage. Skin pigmentation is determined by melanin levels, with fair-skinned individuals having less eumelanin and thus higher UV sensitivity and cancer risk. UV radiation is divided into UVA, UVB, and UVC, with UVA penetrating deeper into the skin and UVB causing direct DNA damage. UV exposure varies geographically and is influenced by factors such as altitude, cloud cover, and latitude. Indoor tanning increases UV exposure and skin cancer risk, with significant increases in melanoma risk for those who tan before age 35. UV-induced DNA damage leads to mutations and cancer, with the NER pathway playing a critical role in DNA repair. Xeroderma Pigmentosum, a genetic disorder, results from NER deficiencies and leads to severe UV sensitivity and skin cancer. The melanocortin 1 receptor (MC1R) is a key gene involved in pigmentation, tanning, and skin cancer susceptibility. MC1R polymorphisms are associated with fair skin, sun sensitivity, and increased melanoma risk. MC1R signaling enhances melanin production and DNA repair, reducing UV-induced damage. Pharmacologic manipulation of cAMP levels may help reduce UV sensitivity and cancer risk. Overall, UV exposure is a major risk factor for skin cancer, and minimizing UV exposure is crucial for reducing skin cancer incidence.