An example is detailed in our recent report of a patient with refractory progressive colorectal cancer which was mismatch-repair (MMR)-deficient, KRAS wild-type, and BRAFV600E-mutant, who appeared to benefit from a small-molecule BRAF inhibitor (14) only when an epidermal growth factor receptor (EGFR) inhibitor was co-prescribed to block this interfering anti-apoptotic pathway (15). This evidence concerns the gene KRAS and colorectal cancer.