So far, studies in ventricular cardiomyocytes revealed that LMNA mutations result in cytoskeletal and microtubule disruption (44, 47), dysmorphology of the nuclei (42), activation of the DNA damage response (48) and PARP1 activation (49, 50) followed by consumption of mitochondrial NAD+ levels, which drive cardiomyocyte dysfunction and cardiomyopathy onset (49, 51). This evidence concerns the gene LMNA and cardiomyopathy.