Cancer is an environmental disease and skin cancer (melanoma and non-melanoma) is the most common of all cancers. Epidemiological and experimental evidence suggest "chronic inflammation" to be one of the hallmarks in solar ultraviolet radiation and several other environmental agent-mediated skin cancers. The identification of transcription factors, mainly nuclear factor-kappa B (NF-κB), signal transducer and activator of transcription 3 (STAT3), hypoxia-inducible factor-1 alpha (HIF-1α) and their gene products i.e. prostaglandins, cyclooxygenase-2 (COX-2), cytokines [tumor necrosis factor- alpha (TNF-α)], chemokines [CXC-chemokine ligand (CXCL)] and chemokine receptors suggest critical role of inflammation in skin carcinogenesis. Considering the potential role of inflammation in tumor initiation and its major role in promotion/progression, as well as tumor angiogenesis and metastasis; inflammatory pathways may become attractive targets for skin cancer prevention. Hence this review focuses on compiling available evidence and understanding the role of chronic inflammation in the development of skin cancer.