As Gramlich et al demonstrated that exposure of mice with truncated titin to isoproterenol or angiotensin-II (AT-II) mimic typical features of DCM—left ventricular dilatation with impaired fractional shortening [30], we investigated whether the mutated and healthy cardiomyocytes respond differently to the following positive inotropic interventions: (1) β-adrenergic stimulation by isoproterenol; (2) elevated [Ca2+]out; (3) AT-II. This evidence concerns the gene TTN and familial dilated cardiomyopathy.