Ultraviolet radiation (UVR) exposure is well established as the major environmental risk factor for the development of melanoma, cutaneous squamous cell carcinoma (cSCC), and basal cell carcinoma (BCC). Additional risk factors including genetic mutations, other environmental agents, and immune status are important in modulating the effects of UVR. Dermatologists advocate a multi-pronged approach to minimizing UVR exposure including lifestyle modifications, UVR protective clothing, and topically applied sun-protective products, i.e. sunscreen. New Federal Drug Administration (FDA) regulations on sunscreen have brought certain long-standing ingredients in sunscreen products under scrutiny. The FDA's proposed rule for over the counter (OTC) monograph states that the inorganic sunscreens, zinc oxide and titanium dioxide, were found to be "generally recognized as safe and effective," but cite insufficient evidence to grant organic sunscreens the same designation. This proposed rule by the FDA and our increasing understanding of multifactorial mechanisms of UVR damage are an impetus for innovation and advances in sun protective technology. A complete set of strategies designed to limit the risk of UV-induced skin cell malignant transformation and tumor development must address the fuller consideration of genetic, environmental, and immune factors that cooperatively drive cutaneous carcinogenesis. Recent advances in our understanding of the biochemical processes underpinning UVR associated cutaneous cellular damage, genotoxicity, and clonal expansion provide investigators with a spectrum of opportunities for technologic innovation in the prevention of skin cancer. Strategies to improve upon current topical sunscreen formulations have strived for broader UVR spectral coverage, more favorable aesthetics, increased adherence, and minimal penetration into the living epidermis. In addition to improved sunscreens, future topical therapies may target processes within the epidermis that contribute to carcinogenesis. These include reactive species quenching, delivery of DNA repair enzymes, and targeting of cytokines essential to the proliferation of mutant keratinocytes.