Of note, both fenofibrate-mediated PPARα activation in vitro (Figure 1) and genetic deletion of PPARα in vivo (Figure 2) prevented PE- and TAC-induced cardiomyocyte hypertrophy, respectively, which was inhibited by either pharmacological (Figure 1) or genetic perturbation (Figure 2) of Nox2, respectively. Here, CYBB is linked to persistent truncus arteriosus.