MSH6 and glioblastoma: Our prospective genomic profiling of 459 consecutive primary treatment-naïve IDH-wildtype glioblastomas within the cerebral hemispheres of adults identified a distinct subgroup defined by the combination of somatic hypermutation (TMB of ≥ 15 somatic mutations per Mb) and biallelic inactivation of a canonical mismatch repair gene (MSH2, MSH6, MLH1, or PMS2) with loss of the affected mismatch repair protein by immunohistochemistry (Table 1, Supplementary Tables S1 and S2).