Since Gonzalez-Villalobos et al. [67] have demonstrated that ACE-mediated ANG II formation is important for the progressive increase in intrarenal ANG II levels and the development of hypertension, one can assume that 20-HETE receptor antagonist diminished the ACE activity leading to the reduction in ACE-mediated ANG II generation and the suppression of the intrarenal ANG II levels. This evidence concerns the gene ACE and hypertensive disorder.