As such, additional research is urgently needed to delineate the exact molecular mechanisms behind PRMT5’s interactions with the ERK1/2 and PI3K pathways, as well as the specificity of these findings in KRAS-mutant CRC, as this can aid in the development of much needed therapeutic strategies to target PRMT5 and the ERK1/2 and PI3K pathways in CRC. This evidence concerns the gene KRAS and colorectal carcinoma.