Different from V600E mutant BRAF cells, many existing BRAF inhibitors paradoxically activate RAF and ERK signalling via a RAS dependent mechanism in wild type BRAF cells.8 Furthermore, malignant tumours with V600E mutant BRAF do not respond uniformly to BRAF-targeted therapy.9 The majority of colorectal cancer patients harbouring V600E mutant BRAF display inherent resistance to vemurafenib. This evidence concerns the gene BRAF and colorectal cancer.