In light of the previously mentioned, precedent-setting use of a toxicity pathway based upon p53 tumour-suppressor functions as a basis for dose-response assessment, particular attention has been given in this review to epigenetic controls regulating (silencing) the expression of the archetypal INK4B-ARF-INK4A-pRB (inhibitor of cyclin-dependent kinase 4B; ADP-ribosylation factor; inhibitor of cyclin-dependent kinase 4A; retinoblastoma protein) tumour suppressor pathway as a mechanism in oncogenic transformation of human cells. The gene discussed is TP53; the disease is neoplasm.