Moreover, using different methods such as immunofluorescence, immunohistochemistry, q-PCR, proteomics and next-generation sequencing (NGS) in several cancer types, we demonstrated that VDAC1 depletion in tumors resulted in major changes in the expression of metabolism-related enzymes such as glucose transport, glycolysis, the TCA cycle, electron transport, and ATP synthesis, and also affected epigenetic modifications involving mitochondrial metabolite-dependent processes [41,45,46,47,48,49,50,51,52]. The gene discussed is VDAC1; the disease is cancer.