Although nuclear fragility secondary to lamin A/C-insufficiency has been postulated to render cardiomyocytes more susceptible to mechanical stress-induced damage and apoptosis [29], the application of mechanical stress to lamin A/C-insufficient (LMNA+/−) mice failed to enhance apoptosis or accelerate DCM.[30] On the contrary, histological studies of the hearts of both lamin A/C-insufficient (LMNA+/−), and lamin A/C-deficient (LMNA−/−) mice revealed typical nuclear abnormalities and apoptosis in cardiomyocytes. The gene discussed is LMNA; the disease is familial dilated cardiomyopathy.