Based on their findings, they demonstrated that CYP1B1 contributes in the development of hypertension most likely by increased generation of ROS, ERK1/2, and p38 MAPK activity; vascular hypertrophy; endothelial dysfunction; and increased vascular reactivity.59 The same research group further elaborated this phenomenon and evaluated the role of CYP1B1 in the gender difference in response to Ang II-induced hypertension in wild type Cyp1b1+/+ and Cyp1b1−/− female mice. This evidence concerns the gene CYP1B1 and endothelial dysfunction.