However, considering that the mitochondrial potential could be modulated by MTDs through several pathways unrelated to VDAC [108,109], such as promoting apoptosis by inducing MOM permeabilization in neuroblastoma cells and isolated mitochondria [110], inhibiting mitochondria biogenesis [111], or inducing mitochondrial network fragmentation [112], the genetic evidence of VDAC’s involvement in the modulation of the mitochondrial potential by MTDs was required. The gene discussed is VDAC1; the disease is neuroblastoma.