In GBM, SREBP1 cleavage is activated by the mutant EGFR signaling but is insensitive to rapamycin64, which suggests an emerging key function of mTORC2, or is rapamycin-resistant, despite such mTORC1-dependent mechanisms as 4E-BP1 signaling in GBM lipid metabolism reprogramming. This evidence concerns the gene EGFR and glioblastoma.