It is more likely that tumors with the A59T variant and no evidence of dMMR/MSI-H or other coalterations, such as ARID1A, POLE, etc., behave biologically and clinically as one would expect from the general pool of mutant KRAS CRC tumors (i.e., resistant to EGFR inhibition). The gene discussed is KRAS; the disease is colorectal carcinoma.