HADHA and neoplasm: In cancer, MDSCs adapt to the anoxic tumor microenvironment by upregulating mechanistic target of rapamycin (mTOR) and HIF-1α signaling, as well as expression of lipid uptake scavenger receptors (e.g., CD36 and macrophage scavenger receptor 1 [MSR1]) and key fatty acid oxidation enzymes (e.g., CPT1A, acyl-CoA dehydrogenase medium chain [ACADM], hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit alpha [HADHA], and peroxisome proliferator-activated receptor coactivator 1 beta [PGC-1β]) (61–64).