“…In fact, overexpression of other receptor tyrosine kinases (RTKs), or inhibition of neurofibromatosis 1 (NF1) function are also very common in gliomas. They all drive the chronic stimulation of Ras signaling to drive cellular proliferation and migration (Furnari et al, ; Gray, Lewis, Maher, & Ally, ). Other frequent genetic lesions include the loss of phosphatase and tensin homolog ( PTEN ), which antagonizes the phosphatidylinositol‐3 kinase (PI3K) signaling pathway, and activating mutations in PI3KCA , which encodes the p110a catalytic subunit (Furnari et al, ; Gray et al, ; von Deimling, Louis, & Wiestler, ).…”