The pathophysiology involves catecholamine-mediated myocardial stunning, with circulating epinephrine levels 2–3 times higher than in myocardial infarction patients, triggering Beta-2 (β2) adrenergic receptor switching from stimulatory G protein (Gs) to inhibitory G protein (Gi) coupling, resulting in negative inotropy [5]. The gene discussed is GNAI1; the disease is myocardial infarction.