Moreover, the identification of SMYD3 as a novel key co-factor for c-MYC cancer-promoting functions opens new avenues for taking advantage of the indirect inhibition of an “undruggable” factor such as c-MYC80 and suggests that this pharmacological strategy may efficiently target the SMYD3/c-MYC axis in CRC. This evidence concerns the gene MYC and colorectal carcinoma.