Indeed, additional events are required to trigger tumour formation, including mutation-driven inactivation of tumour suppressor genes as mentioned above [157–160], its silencing through promoter hypermethylation [164] or the downregulation of the lnk4a/Arf locus expression to prevent the senescence programme, leading to uncontrolled proliferation in reprogrammed SCs [165]. The gene discussed is CDKN2A; the disease is neoplasm.