Using a skin carcinogenesis model with 7,12-dimethyl benz(a)anthracene (DMBA) and TPA in TRPV1−/− (knockout) and TRPV1+/+ (wild type) mice, authors have shown that TRPV1−/− mice developed significantly more skin tumors than TRPV1+/+ mice [73]. This evidence concerns the gene TRPV1 and neoplasm.