Regarding MM therapeutics, inhibiting hexokinase (HK) activity, which converts glucose to glucose-6-phosphate, driving tumor glycolysis, by using antisense oligonucleotides, may effectively inhibit HK1-HK2+ MM cell proliferation, while combining HK2 inhibition with partial oxidative phosphorylation inhibitions may show promising results in eliminating MM progression [112]. Here, HK2 is linked to Miyoshi myopathy.