Previous studies have identified improved outcome with addition of anti‐epidermal growth factor receptor (EGFR) therapy to chemotherapy in CRC patients with RAS wild type.4, 5 However, mutation of RAS family or BRAF may activate the downstream RAS‐RAF‐MAPK pathway, which is independent of EGFR inhibition, and associated with resistance to anti‐EGFR therapy.6 Hence the mutation profiles may help to select candidates for optimal therapy. Here, BRAF is linked to colorectal carcinoma.