While EGFR and PDGFRA amplifications are the major genomic abnormalities in classical and proneural GBMs, respectively, deficiency in NF1, mainly via homozygous and hemizygous deletions, was observed as a highly frequent event in mesenchymal GBMs, and the pathobiological significance of such loss was associated with the infiltration of TAMs into the tumor microenvironment followed by PMT and radioresistance [11, 130, 155, 161]. Here, NF1 is linked to neoplasm.