Initially, it was believed that the attenuation of myocardial contractility and reduction in heart rate resulting from β1 receptor blockade were crucial mechanisms for preventing plaque rupture by decreasing blood flow shear stress and minimizing damage to the vascular endothelium (Kaplan and Manuck, 1994), However, subsequent findings revealed that even after adjusting for mean heart rate during treatment, the association between β-AR blockers and a reduced rate of atherosclerosis progression remained statistically significant. The gene discussed is ADRB2; the disease is atherosclerosis.