Interestingly, our laboratory reported that PRMT5-catalyzed dimethylation on R30 of the NF-κB p65 subunit and R205 of YBX1 promotes cell proliferation, migration, and anchorage-independent growth in CRC, suggesting the versatility of a PRMT5-regulated substrate in CRC tumors [31,60]. The gene discussed is PRMT5; the disease is colorectal carcinoma.