The study was conducted on mice with a knockout of MR in T cells and HTN induced by Ang II, demonstrating that the deficiency of MRs in T cells decreases both the systolic and diastolic BP, pre-existing vascular damage, and the levels of IFNγ originating from T cells in the kidneys and aorta [43], thus showing that the inflammation produced by the activation of T cells is related to the development of HTN. Here, IFNG is linked to hypertensive disorder.