Psarras S. et al. determined an increase of the posterior left cardiac ventricular wall thickness by 30% together with an increase of the systolic left cardiac ventricular function by 53% and a decrease of the left cardiac ventricular dilation by 29% with almost normalized end-diastolic diameter values in OPN-/- mutated mice with dilatative cardiomyopathy [38], further proving OPN’s role in adverse cardiomyocyte remodeling and pathological changes of cardiac ventricular geometry. The gene discussed is SPP1; the disease is dilated cardiomyopathy.