In the present study, we showed that PRMT5 not only overexpressed in colorectal cancer cells and tissues (Figure 1), but also regulated cell cycle progression and promoted cell growth via regulation of cyclin D1, cyclin E1, and p27, using PRMT5 stable knockdown cell lines and specific inhibitor GSK591 (Figures 2, 3), which was associated with PRMT5 enzyme activity. Here, CCND1 is linked to colorectal cancer.