Some of the most convincing evidence for epigenetic disruption of progenitor cells derive from the ubiquitous nature of genome-wide hypomethylation in almost all cancers, common hypermethylation of genes, such as p16INK4a, in many cancer types (and, occasionally, in surrounding normal tissues) and ‘germline epimutations’, such as heightened loss of imprinting (LOI) of insulin-like growth factor 2 in patients at risk for colorectal cancer (Feinberg et al, 2006). Here, CDKN2A is linked to cancer.