VDAC1 contributes to cancer metabolism via transport of various metabolites, mediating ATP/ADP exchange across the OMM and is, therefore, defined as the “food channel.” HK, by association with VDAC1, gains direct access to mitochondrial ATP, reaching VDAC1 via the ANT in the IMM, allowing it to phosphorylate and “trap” any incoming glucose (Pedersen, 2008). Here, HK1 is linked to cancer.