Both DNMT3A and TET2 have been shown to prevent DNA hypermethylation of canyons and promoter CGIs, suggesting that de novo methylation and 5hmC formation by DNMT3A and TET2 work simultaneously in HSPCs to prevent specific tumor suppressor gene loci from becoming dysregulated, and their potential cooperation at these sites requires further study. The gene discussed is TET2; the disease is neoplasm.