For example, hyperactivation of NRF2 as a result of KEAP1 loss-of-function protected from UV-induced skin carcinogenesis [70,71], while mice expressing low levels of caNRF2 in keratinocytes showed increased tumor incidence and multiplicity in a genetic model of Human Papilloma Virus 8-induced skin cancer, resulting primarily from increased survival of keratinocytes during the early stages of the transformation process [72]. Here, NFE2L2 is linked to neoplasm.