Since a number of LMNA mutations result in a loss of function, lamin A/C haploinsufficient (Lmna+/−) and Lmna knockout mice (Lmna-/-) have been extensively used to study the molecular mechanisms underlying LMNA loss-of-function (LOF) cardiomyopathy (Table 2). Here, LMNA is linked to cardiomyopathy.