A number of post-translational modifications on TET2 have been reported, including oxidative stress,36 diabetes,37 immunity,34,38 and cancer.20,37 Phosphorylation orchestrates ubiquitination is the most common mechanism of protein stability regulation which execute the upstream signal transduction.24 Wu et al. showed that increased glucose levels impede AMPK-mediated phosphorylation at TET2 serine 99 which leads to the destabilization of TET2.37 In this study, we reported that protein kinase MEK1 phosphorylated TET2 at serine 1107 preventing proteasome degradation of TET2. The gene discussed is MAP2K1; the disease is diabetes mellitus.