Proteins at cell-cell junctions (e.g., Cx43) and within distinct regions of the sarcomere were major targets for altered phospho-dependent regulation, implying that DCM occasioned by ErbB2 inhibition involves decreased mechanical coupling and electrophysiological properties as well as sarcomeric dysfunction via altered structural assembly and force. The gene discussed is ERBB2; the disease is familial dilated cardiomyopathy.