Experimental glioma dedicated work has reproduced these molecular relationships and shown functional consequences relevant to therapy: overexpression of beclin-1 in U87 GBM cells increases autophagic flux and, in some contexts, augments apoptosis, whereas beclin-1 knockdown reduces autophagy and alters treatment responses, indicating context-dependent pro-survival versus pro-death roles. Here, BECN1 is linked to central nervous system cancer.