Previous study in a lamin A-haploinsufficiency mouse model of DCM had suggested that reduction of lamin A/C proteins render premature apoptosis, particularly in electrically active cardiomyocytes [18.] Therefore, we applied electrical stimulation to cultured dermal fibroblasts to simulate an in-vivo cardiac electric field, and scored the fractions of abnormal nuclei present in control and LMNAR225X/WT dermal fibroblasts (Figure 3A-D). The gene discussed is LMNA; the disease is familial dilated cardiomyopathy.