Preventing the metabolism of EETs to DHETs by inhibiting the sEH prevented AngII-induced cardiac hypertrophy, in fact, there is a lot of evidence linking AngII with increased sEH expression.172 In a TAC mouse model, beneficial effects of sEH inhibition were noted in the prevention of ventricular arrhythmias that occur in association with cardiac hypertrophy.173 Similarly, sEH-deficient mice that underwent either TAC- or Ang II-induced hypertrophy demonstrated preserved cardiac function compared to controls. This evidence concerns the gene AGT and persistent truncus arteriosus.