ADRB2 and familial dilated cardiomyopathy: Studies by this and other groups have demonstrated that cardiac overexpression of β1‐AR, β2‐AR, stimulatory G‐protein, or protein kinase‐A, all resulted in similar DCM phenotypes (Dorn 2nd et al., 1999; Du, 2001; Du, Gao, Wang, et al., 2000; Engelhardt et al., 1999), implying an adverse class effect of enhanced β‐adrenergic signaling.