Although this phenomenon is universal to many cell types with abnormal A-type lamin composition [20], [28], [29], [30], the administration of the MEK inhibitor, PD98059, improves the dilated cardiomyopathy of LmnaH222P/H222P mice [31], [32], which strongly supports the notion that altered ERK1/2 activity is a critical component associated with pathogenesis. Here, LMNA is linked to dilated cardiomyopathy.