This composite design captures the clinical phenotype of T2DM-AMI patients with ALI—typically older, with higher rates of STEMI, anterior infarction, arrhythmias, and hypertension—while mechanistically explaining the detrimental interplay between neutrophilic activation (e.g., myeloperoxidase-driven oxidative stress) and hypoalbuminemia (reflecting hepatic synthetic impairment and diminished antioxidant capacity). The gene discussed is MPO; the disease is Hypoalbuminemia.