EGFR amplification/mutation and mTOR mutations may be significant resistance mechanisms associated with BRAF-targeted therapy, as signalling through the EGFR/PI3K/AKT/mTOR cascade overcomes the block on BRAF/MEK to continue cell proliferation.116 This phenomenon should be explored further to identify the specific subsets of BRAF-mutant glioblastoma patients that may benefit from BRAF/MEK therapy alone and to clarify whether the addition of EGFR or mTOR inhibitors is required for BRAF-resistant tumours. This evidence concerns the gene MTOR and neoplasm.