EGFR and colorectal cancer: BRAF inhibitor monotherapy has not yielded clinically significant improvements,14, 15 however, likely due to compensatory feedback reactivation of EGFR mediated mitogen-activated protein kinase signalling pathways, a well documented mechanism for resistance in preclinical models.16, 17 Subsequently, the finding of EGFR mediated feedback activation has driven the exploration of dual EGFR/BRAF blockade in BRAF-mutated colorectal cancer.