For example, in cells with wild type BRAF, BRAFi binding to one BRAF protomer in a BRAF:BRAF or BRAF:CRAF dimer results in allosteric activation of the non-drug-bound dimer partner resulting in paradoxical activation of ERK1/2 signalling and adventitious tumour growth in non-melanoma tissue [44]. This evidence concerns the gene RAF1 and neoplasm.