In glioblastoma, EZH2 can be phosphorylated at Ser21 by protein kinase B (AKT), leading to the methylation of STAT3 and the consequent activation of this signaling pathway [69,70,71], and in castration-resistant PCa (CRPC), phosphorylated EZH2 activates the androgen receptor (AR) via a non-catalytic mechanism directly occupying the AR promoter and activating downstream genes [71] (Figure 1). This evidence concerns the gene AKT1 and glioblastoma.