Given that the SMARCA4-R1157W mutant promotes CRC cell proliferation by enhancing the binding to PRMT1-mediated H4R3me2a and chromatin remodeling activities of the SWI/SNF complex, we sought to examine whether the combined inhibition of PRMT1 and SMARCA4 ATPase activity would yield a favorable therapeutic effect on SMARCA4-R1157W mutant CRC. This evidence concerns the gene SMARCA1 and colorectal carcinoma.