CDKN2A and neoplasm: The presence of oxidative DNA damage could also contribute to pro-oncogenic events within the microenvironment, favoring aberrant DNA methylation in target cells [38], with hypermethylation of Cdkn2a (Ink4a/Arf) in LNT- and LFA-induced lesions prior to tumor development leading to allelic loss of p19Arf, as has been suggested in other cancers [17].