Furthermore, in colorectal cancer cells with double knockout of endogenous AKT1 and AKT2, the ability of PRMT5 to activate the AKT/mTOR signaling pathway was rescued when AKT1 expression was restored with wild‐type AKT1 but not the AKT1 R391K mutant (which contains a mutation blocking its PRMT5‐mediated methylation [27]) (Figure 4I,J; Figure S7B–D, Supporting Information). The gene discussed is AKT1; the disease is colorectal cancer.