KEAP1 and neoplasm: The role of NRF2 as the mediator of the protective effects of TBE-31 against tumor development is further strengthened by the fact that genetic (by KEAP1 knockdown) or pharmacological (by small quantities of TBE-31, administered topically twice a week) activation of NRF2 reduces inflammation and photocarcinogenesis in the skin of SKH-1 hairless mice exposed to ultraviolet (UV) radiation24, and the protective effect of the KEAP1 knockdown is abrogated when NRF2 is deficient25.