Sodium (SCN5A), and potassium (ABCC9, KATP) channel regulation defects have also been associated with the development of DCM, which argues for an alternative disease mechanism of dilatation-induced remodeling that is mainly driven by a dysfunction in an electrical excitability component rather than a primary structural defect (6, 7). The gene discussed is SCN5A; the disease is familial dilated cardiomyopathy.