Whole-exome sequencing of recurrent GBM suggests that these tumors arise from residual primary tumor cells, supporting a model of evolutionary adaptation to treatment.181 Tumor heterogeneity influences differential treatment responses, particularly the expression of key biomarkers such as MGMT and RTKs.182,183 Studies have revealed that mixed tumor cell populations with distinct RTK amplifications, including EGFR, MET, and PDGFRA, contribute to therapeutic resistance.184. The gene discussed is MET; the disease is glioblastoma.