BCL2 and glioblastoma: GBM–EVs overexpressing linc-CCAT2 from the U87 GBM cell line were indeed reported to enhance EC expression of VEGF-A and transforming growth factor-beta (TGF-β) while inhibiting apoptosis via activating B cell lymphoma-2 (Bcl-2) and suppressing Bcl2-associated protein x (Bax) and caspase-3 in vitro [27].