STAT3 and neoplasm: In GSCs rather than non-stem bulk tumor, AKT induces EZH2 phosphorylation at Ser21 and this so-called “phospho-switch” of EZH2 (see Section 4) enhances its interaction with STAT3, which is followed by STAT3 lysine-180 trimethylation by EZH2, resulting in increased tyrosine phosphorylation and activation of STAT3 [39].