Furthermore, MA-TAMhigh tumors were marked by frequent genomic ablations of NF1 and PI3K pathway components, indicating the essential role of pathogenic activation of downstream effectors mediated by loss of NF1 and PI3K/AKT/mTOR signaling in GBM tumor cells for the induction and maintenance of MA-TAMs in GMB tumor microenvironment [4, 46, 48–50]. This evidence concerns the gene AKT1 and glioblastoma.