In our previous studies, we found that PRMT1-mediated H4R3me2a (ω-NG, NG-asymmetric dimethylation of the guanidine nitrogen of Arg 3 in histone H4) recruits the wild-type SMARCA4 to promote colorectal cancer progression by enhancing EGFR signaling, providing another example of an oncogenic role of SMARCA4 in CRC23. The gene discussed is SMARCA4; the disease is colorectal cancer.