A total of six prior published clinical trials report molecular results of tumour tissue and circulating free DNA (cfDNA) in patients with BRAFV600E mutated metastatic CRC receiving therapies consisting of a backbone of BRAF and EGFR inhibition or BRAF inhibition monotherapy.7,10,13,18,23,24 No difference in outcome was described between microsatellite stable and instable tumours in this cohort nor in literature.7,12,13 The genetic alterations identified for acquired resistance arose in genes directly or indirectly activating signalling via the MAPK pathway or cross-linked pathways. The gene discussed is BRAF; the disease is neoplasm.