Studies on patients and lamin A/C–deficient mouse models indicate that loss of function of lamin A/C proteins also develops some of the laminopathies, including muscular dystrophy, dilated cardiomyopathy (DCM), and Charcot–Marie–Tooth disorder, type 2 (CMT2) [14,23,24]. The gene discussed is LMNA; the disease is familial dilated cardiomyopathy.