Further studies showed that co-treatment with melatonin and 3-MA prominently decreased the expression of the anti-apoptotic protein, bcl-2, whereas the expression of an apoptosis-promoting protein, Bax, was significantly increased, which collectively indicated that the disruption of autophagy triggers the melatonin-induced apoptosis in glioblastoma cells (Fig. 8). The gene discussed is BCL2; the disease is glioblastoma.