In previous studies across various cancer mouse models, including lung, bladder, breast cancers, glioblastoma, and mesothelioma, silencing VDAC1 expression reversed oncogenic properties, including reprogrammed metabolism, inhibited angiogenesis, epithelial-to-mesenchymal transition (EMT), invasiveness, and stemness [17,18,19,20,21,22,23,28,29,30,51]. The gene discussed is VDAC1; the disease is glioblastoma.