VDAC1 and cancer: As discussed above, interaction of HXKII with VDAC in MOM allows HXKII to have preferential access to ATP, so inactivation and dissociation of HXKII from MOM implies a reduction in glycolytic flux and leads to interaction of VDAC to Bcl-protein family, which promotes opening of mPTP and subsequent apoptosis, so chemicals that induce this process could be used to reduce cancer cell proliferation, just as jasmonate does (Goldin et al., 2008).