A previous study showed that increased glucose levels could impede adenosine 5′-monophosphate-activated protein kinase (AMPK)-mediated phosphorylation at serine 99, resulting in the destabilization of tet methylcytosine dioxygenase 2 (TET2), followed by the dysregulation of both 5-hydroxymethylcytosine (5hmC) and the tumor suppressive function of TET2 in vitro and in vivo [30]. The gene discussed is TET2; the disease is neoplasm.