Recent studies have indicated that PRMT5 methylates and activates AKT and consequently increases cancer cell proliferation.[27, 38] Consistent with published studies, the overexpression of PRMT5 activated the AKT/mTOR signaling pathway (Figure4A,B; Figure S6A–F, Supporting Information), whereas the overexpression of PRMT5 R368A (a methyltransferase‐inactive mutant of PRMT5) failed to activate the AKT/mTOR signaling pathway (Figure 4A,B). Here, AKT1 is linked to cancer.