Because around 80% of total HK2 is reported to be bound to the mitochondrial VDAC [107], and because we see elevated levels of HK2 in tumor cells that are exposed to bone marrow adipocytes, it is plausible to expect that the mitochondrial binding of HK2 is occurring in PCa cells, a process that could be promoting tumor cell survival via inhibition of intrinsic apoptosis in response to adipocyte-supplied factors. Here, HK2 is linked to neoplasm.