Transgenic mice with cardiac-specific overexpression of GRK2 had contractile responses to βAR abolished and displayed physiological alterations (e.g., impairment of βAR functions and signaling, and cardiac hypertrophy), resulting in a failing heart in these mice (Koch et al., 1995; Rockman et al., 1998). This evidence concerns the gene ADRB2 and cardiac hypertrophy.