These consisted of one gliosarcoma case with NRAS Q61K gain of function mutation, one superficial glioblastoma case with oligodendroglial-like morphology and BRAF D594N loss of function mutation that nevertheless activates ERK/MAPK through activation of cRAF [22], and eight cases with NF1 pathogenic mutations, two of which also containing an additional MTOR splice region variant of unknown significance (A1971V; NM004958) or a TSC2 in frame deletion/insertion (S1282-G1285 delinsR; NM 000548). Here, NF1 is linked to glioblastoma.