More recently, it has been shown that the acetyl coenzyme A (acetyl-CoA) derived from glucose and lactate metabolism is used by GBM cells to induce RICTOR acetylation that results in mTORC2 activation; this mechanism creates an autoactivation loop by which mTORC2 triggers cell proliferation and growth, bypassing growth factor-activated upstream signaling and rendering GBM cells resistant to receptor tyrosine kinase inhibitors [30]. This evidence concerns the gene RICTOR and glioblastoma.