Further, KRAS upregulated FUBP1 through inhibition of caspase 3‐dependent cleavage, as well as the decrease in Smurf2, which promotes ubiquitin‐mediated degradation accounted for the increase in FUBP1 in both KRAS wild‐type and mutated CRC patients. This evidence concerns the gene FUBP1 and colorectal carcinoma.