Shimizu et al. (2000) and Talaska et al. (2006) found that compared with the wild type, the Ahr−/− mice did not develop subcutaneous or skin tumors in response to BaP exposure and had a 90% reduction in BaP adduct levels. Fan et al. (2010) showed that Ahr−/− mice exposed to diethylnitrosamine had an elevated incidence of liver tumor formation compared with the wild type. Diethylnitrosamine is a potent hepatic carcinogen but is not an agonist for the AHR. These data suggest that in the absence of a xenobiotic ligand, the Ahr gene can function as a tumor suppressor gene. This evidence concerns the gene AHR and Neoplasm of the liver.