The pro-inflammatory milieu interferes with blood pressure regulatory mechanisms, such as the renin–angiotensin system and the sympathetic nervous system [113]; in particular, circulating TNF-α, which is increased in patients with SLE and correlates with disease activity, is involved in the development of hypertension; indeed, in female murine models of SLE, a decrease in mean arterial pressure has been observed after treatment with the anti-TNF-α antibody etanercept [114,115]. Here, TNF is linked to Hypertension.