Photocarcinogenesis is multistage process of initiation, promotion and progression. A conventional knowledge demonstrated that accumulation of genetic mutation caused by UV leads to the development of skin cancers. UVB (and UVA) causes the formation of dipyrimidine photoproducts or oxidative DNA damage, such as 8-oxo-7,8-dihydroguanine (8-oxoG) in skin cells, resulting in the alteration of the genes involved in cancer related genes and development of skin cancers. This is true but recent findings revealed an important role of infammation in the process of photocarcinogenesis. It became evident that DNA damage and infammation is closely related. A damage itself trigers the signaling pathway and modulation of gene expression and causes inflammation. In Ogg1 knockout mice, which fail to repair 8-OxoG, manifest much higher frequency of UV-induced skin cancers without the increase in p53 gene mutation, and in this system the presence of 8-oxoG upregulates inflammatory genes and promote skin cancer development. Furthermore we have shown that mice model of xeroderma pgimentosum (XP), hereditary DNA repair disorder, where patietns manifest severe sunburn and high frequency of skin cancers in ear age, expressed exteremely high level of CXCL1 and, to our surprise, inihibiting CXCL1 with neutral antibody markedly decreased the development of UV-induced skin cancers, without the change in repair of dipyrimidine photoproducts. These data imply that the presense of DNA damage contribute to the occurrence of inflammation in addition to gene mutations. Inflammation causes oxidative DNA damage again, which vicous cycle may give a big impact on cancer development. We also investigated the mecahnisms how UV-induced inflammation is resoluted. After UV exposure, keratinocutes go into apoptosis, follwed by the phagocytosis by Langerhans ells, where interaction between phagocytosed apoptotic cells modulate the gene expression and lead to the resolution of inflammation.