Moreover, in colorectal cancer cells with double knockout of endogenous AKT1 and AKT2, the ability of PRMT5 to increase cell proliferation and promote colorectal cancer liver metastasis 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 5G,H). This evidence concerns the gene PRMT5 and colorectal cancer.