Namely, age, presence/absence of comorbidities (T2DM and CKD), and weight loss, taken together, explained a fair share of myocardial ischemia and inflammation improvements (41% of H-FABP, 31.5% of cardiac troponin, and 39.7% of fibrinogen reduction from phase I to phase II). The gene discussed is FABP3; the disease is myocardial ischemia.