Here, we found that the overexpression of PRMT5 increased the proliferation of colorectal cancer cells (Figure5A,B) and that the effect of PRMT5 on colorectal cancer cell proliferation was reversed by treatment with rapamycin, a selective mTOR inhibitor [43] that suppresses the AKT/mTOR signaling pathway (Figure 5A,B). The gene discussed is AKT1; the disease is colorectal cancer.