Ultraviolet (UV) radiation plays a crucial role in the development of both melanoma and non-melanoma skin cancers. UV radiation is categorized into UVA (315 to 400 nm), UVB (280 to 320 nm), and UVC (100 to 280 nm) based on wavelength. UV radiation can cause direct DNA damage through the formation of cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs), as well as indirect DNA damage through photosensitization reactions that produce reactive oxygen species (ROS) and 8-hydroxy-2′-deoxyguanine (8-OHdG). These damages can lead to mutations in genes such as BRAF and NRAS, which are significant risk factors for melanoma development. UV radiation also influences the development of basal cell carcinoma (BCC) by causing mutations in the Hedgehog (Hh) pathway and promoting cell proliferation and survival. Additionally, UV radiation can induce squamous cell carcinoma (SCC) via mutations in the TP53 gene and upregulation of matrix metalloproteinases (MMPs) in the stroma layer of the skin. The ozone layer, which absorbs much of the sun's UV radiation, acts as a critical barrier. However, human activities have weakened this layer, increasing the risk of UV radiation reaching the Earth's surface. This has led to an increase in skin cancer incidence, particularly in regions with high UV exposure. UV radiation can cause photoaging and increase the risk of skin cancer through various mechanisms, including the activation of pathways like mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB), which elevate MMP levels. Photolyases, which repair UVB-induced DNA damage, are absent in mammals, leading to reliance on the nucleotide excision repair (NER) system. Melanoma, the most lethal form of skin cancer, is significantly influenced by the signaling of the melanocortin one receptor (MC1R), which regulates melanin synthesis. Mutations in the BRAF and NRAS genes are common in melanoma development. Treatment options for melanoma include targeted therapies that inhibit BRAF and MEK, as well as checkpoint inhibitor immunotherapy. BCC, the most common form of skin cancer, is primarily caused by intense intermittent UV exposure and genetic modifications in the Hh signaling pathway. Mutations in the PTCH1 and SMO genes are prevalent in BCC, leading to increased Hh pathway activation. TP53 mutations are also frequent in BCC, contributing to cell proliferation and survival. Treatment options include surgical excision, Mohs micrographic surgery, photodynamic therapy, and pharmacological inhibitors targeting the Hh pathway. SCC, the second most common non-melanoma skin cancer, is primarily causedUltraviolet (UV) radiation plays a crucial role in the development of both melanoma and non-melanoma skin cancers. UV radiation is categorized into UVA (315 to 400 nm), UVB (280 to 320 nm), and UVC (100 to 280 nm) based on wavelength. UV radiation can cause direct DNA damage through the formation of cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs), as well as indirect DNA damage through photosensitization reactions that produce reactive oxygen species (ROS) and 8-hydroxy-2′-deoxyguanine (8-OHdG). These damages can lead to mutations in genes such as BRAF and NRAS, which are significant risk factors for melanoma development. UV radiation also influences the development of basal cell carcinoma (BCC) by causing mutations in the Hedgehog (Hh) pathway and promoting cell proliferation and survival. Additionally, UV radiation can induce squamous cell carcinoma (SCC) via mutations in the TP53 gene and upregulation of matrix metalloproteinases (MMPs) in the stroma layer of the skin. The ozone layer, which absorbs much of the sun's UV radiation, acts as a critical barrier. However, human activities have weakened this layer, increasing the risk of UV radiation reaching the Earth's surface. This has led to an increase in skin cancer incidence, particularly in regions with high UV exposure. UV radiation can cause photoaging and increase the risk of skin cancer through various mechanisms, including the activation of pathways like mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB), which elevate MMP levels. Photolyases, which repair UVB-induced DNA damage, are absent in mammals, leading to reliance on the nucleotide excision repair (NER) system. Melanoma, the most lethal form of skin cancer, is significantly influenced by the signaling of the melanocortin one receptor (MC1R), which regulates melanin synthesis. Mutations in the BRAF and NRAS genes are common in melanoma development. Treatment options for melanoma include targeted therapies that inhibit BRAF and MEK, as well as checkpoint inhibitor immunotherapy. BCC, the most common form of skin cancer, is primarily caused by intense intermittent UV exposure and genetic modifications in the Hh signaling pathway. Mutations in the PTCH1 and SMO genes are prevalent in BCC, leading to increased Hh pathway activation. TP53 mutations are also frequent in BCC, contributing to cell proliferation and survival. Treatment options include surgical excision, Mohs micrographic surgery, photodynamic therapy, and pharmacological inhibitors targeting the Hh pathway. SCC, the second most common non-melanoma skin cancer, is primarily caused