The steep downregulation of KCNQ1 protein expression (approximately 80%) might have severely compromised the repolarization reserve of the peri-infarct zone cardiomyocytes, which would in turn have led to an increased incidence of ventricular arrhythmias and greater triangulation of MAP in the Infarct (2-d) group under adrenergic stimulation. The gene discussed is KCNQ1; the disease is Ventricular arrhythmia.