In our working model (Fig. 9), the MYC oncogene directly drives the transcription of TET1 (as well as DNMT1 and DNMT3B [26]), while suppressing TET2. Inactivation of MYC inverts the expression pattern of both DNMTs and TETs, eliciting cellular senescence and tumor regression. This evidence concerns the gene DNMT3B and neoplasm.