The investigation of BMCs (BMC1-M1) validated the co-occurrence of MET and NGFR expression in cellular subsets (Supplementary Fig. 5i, j), suggesting that the MET tyrosine kinase receptor pathway may serve as a potent survival and maintenance mechanism in MBM and that the therapeutic targeting by small molecule inhibitors [77] may eliminate several tumor cell fractions including NGFR+ cells potentially featuring resistance to BRAFi. Here, MET is linked to neoplasm.