Taken together, our previous and present results support the thesis that prohypertensive actions of 20-HETE in the vasculature combined with deficiency of antihypertensive effects of 20-HETE and EETs at the tubular level as well as diminished renal vasodilatory action of EETs act in concert to promote the development of ANG II-dependent malignant hypertension, at least its form found in Cyp1a1-Ren-2 transgenic rats. This evidence concerns the gene CYP1A1 and malignant hypertension.