In our work, we confirmed that Prmt5 deficiency reduced the phosphorylation of Akt at Ser473 and inhibited the progression of HCC (Figure 6E), suggesting that Prmt5 depletion inhibits Akt/N-Ras-derived hepatocarcinogenesis, which might partly be due to the dysfunction of methylating Akt1 for oncogenic activation and improving immune dysregulation. The gene discussed is PRMT5; the disease is hepatocellular carcinoma.