We conclude (i) that inhibition of HK2-driven glycolysis, OXPHOS, and FAO is likely to be a pan-tumor precision therapy approach to HK1−HK2+ tumors, regardless of their tissue of origin, and (ii) that cancer therapies that involve HK2 inhibition will be restricted to tumors that do not express HK1. This evidence concerns the gene HK1 and neoplasm.