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. Here, CTCF is linked to neoplasm.