Differently from this, the phosphorylation of EZH2 at Y646 residue by JAK2 promotes the β-TrCP-mediated EZH2 degradation [63] and the phosphorylation on Y244 mediated by JAK3 suppresses PRC2 complex formation, resulting in EZH2 oncogenic function in natural killer/T-cell lymphoma [64]. This evidence concerns the gene EZH2 and T-cell non-Hodgkin lymphoma.