In previous studies demonstrating that Pde9a−/− mice were protected from LV hypertrophy and failure induced by transverse aortic constriction (TAC) (Lee et al., 2015), TAC was associated with more severe ventricular pressure overload, increased expression of ventricular Nppa (not observed here), and ample evidence of LV failure (reduced fractional shortening, LV dilation, interstitial fibrosis). Here, PDE9A is linked to persistent truncus arteriosus.