In contrast to BaP, the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was found to increase Dnmt1 expression/activity which was implicated for the hypermethyation (gain of methylation) of several tumor suppressor genes (e.g. p16ink4A and Rarβ) frequently occurred in both NNK-exposed rodent lung tumors and in smokers who developed lung cancer [33, 43]. This evidence concerns the gene DNMT1 and neoplasm.