More recently using a mouse line that only expresses PKG in smooth muscle cells and cardiac myofibroblasts, investigators have demonstrated that inhibition of PDE5 with sildenafil did not decrease cardiac hypertrophy induced by the infusion of angiotensin II, but did significantly decrease fibrosis suggesting that inhibition of PDE5 in cells other than cardiac myocytes and smooth muscle was responsible for the antifibrotic effect [29]. The gene discussed is PRKG1; the disease is cardiac hypertrophy.