Different from pharmacological inhibition of sEH by TUPS, although EPHX2 deletion resisted the AngII induced hypertension and cardiac hypertrophy, it aggravated the cardiac fibrosis, which has been proposed as a major determinant leading to both cardiac systolic and diastolic dysfunction [46], [47] and contribute to the deterioration of cardiac dysfunction. Here, EPHX2 is linked to cardiac hypertrophy.