CDKN2A and cancer: Thus, the competitive inhibition of KDMs and TETs by oncometabolites induces a typical hypermethylation phenotype [126,130,134,135,136] that affects the transcription of genes involved in DNA repair (MGMT, BRCA, ATM), apoptosis (DAPK, TMS1), cell cycle (p16INK4a, p15INK4b, Rb, p14ARF), carcinogen-metabolism (GSTP1), and cell-adherence (CDH1, CDH13), enabling cancer growth and proliferation [137,138].