BRAFV600E mutant subtype 1 (BM1) harboured KRAS/mTOR/AKT/4EBP1 activation with high levels of immune infiltration and epithelial-mesenchymal transition (EMT) and BRAFV600E mutant subtype 2 (BM2) was mainly dysregulated in cell-cycle checkpoints.17 A higher sensitivity for BRAF, MEK and EGFR inhibition with dabrafenib, trametinib and panitumumab was found in BM1.18 These results suggest that BRAFV600E mutated CRC is indeed a heterogeneous disease with different molecular patterns, responses to and targets for therapy. This evidence concerns the gene BRAF and colorectal carcinoma.