In established mouse models, silencing VDAC1 expression inhibited solid tumor development and growth in cervical, lung, bladder, and breast cancers, mesothelioma and glioblastoma tumors resulted in metabolic rewiring, leading to a reversal of their oncogenic properties, which inhibited tumor growth, invasivity, stemness, epithelial-to-mesenchymal transition (EMT), and angiogenesis [18,19,20,22,23,28]. Here, VDAC1 is linked to breast cancer.