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. This evidence concerns the gene PRMT1 and colorectal cancer.