Further study demonstrated that direct repression of EC-TGFβ1 by simvastatin, through induction of EC-Klf2 or through EC-Klf2 activation of EC-Foxp1, was involved in the reduction of the pathological cardiac fibrosis and hypertrophy in TAC pressure overload induced cardiac dysfunction. The gene discussed is FOXP1; the disease is persistent truncus arteriosus.