The genetic model of cancer – the idea that key mutations lead to unchecked cellular proliferation – has guided cancer research for decades. Thousands of papers report sequence alterations that disrupt, delete, or overexpress genes, leading to oncogenesis. Then, in 1983, Bert Vogelstein and Andrew Feinberg at Johns Hopkins University reported widespread loss of DNA methylation at cytosine-guanine (CpG) dinucleotides in tumor samples.[1] This was the first evidence that eigenetic changes, which are heritable but outside of the genome sequence, might spur cancer.[2] Many remained skeptical, however, regarding the change as an epiphenomenon to primary genetic disruption.[3]