CDKN2A and neoplasm: Given the demonstrated influences that CTCF exerts over epigenetic modifications at the p16/INK4A TSG, it seems likely that carcinogen-induced perturbations of CTCF abundance, as for example by H2O2-induced oxidative stress [244] or interference with CTCF activation by its poly(ADP–ribosyl)ation (see below), could be at the origins of an epigenetic toxicity pathway leading to tumour suppressor gene silencing.