TGFB1 and colorectal carcinoma: Another pathway involved in the development of the EMT subtype is TGF-β, which was probably activated in a minority of patients due to mutations in the SMAD gene.25 Surprisingly, Middleton et al. has shown that the majority of CSM4 subtype BRAFV600E mutant CRC represents a BM1 signature with a better response to combined treatment with dabrafenib, trametinib and panitumumab.18 Unfortunately, it was not feasible to actually determine molecular subtypes BM1 and BM2 in our patient cohort due to restrictions in sequencing data.