For instance, ATR (Ataxia telangiectasia and Rad3-related protein)-mediated phosphorylation of Tet3 promotes changes in 5hmC patterns that is necessary for timely DNA damage responses (57) whereas in vivo tumour-suppressor activity of Tet2 is highly stabilized by AMPK (AMP-activated kinase)-mediated phosphorylation (58). This evidence concerns the gene ATR and neoplasm.