This technology has been taken advantage of in modeling both dilated and hypertrophic cardiomyopathies (DCM, HCM), where point mutations in MYH6, ACTC1, or PRKAG2 cause HCM, and mutations truncating the massive protein titin cause DCM (31, 37–39). The gene discussed is PRKAG2; the disease is familial dilated cardiomyopathy.