In conclusion, after our group’s previous research demonstrated that PRMT5 inhibition shows greater therapeutic effects in KRAS-mutant CRC cells when compared to KRAS WT CRC cells, and that PRMT5 and KRAS may crosstalk, our group sought to determine which key downstream proteins may be mediators of this PRMT5–KRAS crosstalk. This evidence concerns the gene KRAS and colorectal carcinoma.