Muchir et al. reported that mitogen-activated protein kinase (MAPK) signaling is activated in Lmna H222P knock-in mouse (LmnaH222P/H222P) hearts from abnormal activation of extracellular signal-regulated kinase (ERK) and Jun amino-terminal kinase (JNK), and this activation leads to DCM phenotype through actin depolymerization (49, 50). The gene discussed is LMNA; the disease is familial dilated cardiomyopathy.