Downstream of IL-1, IL-6, and CRP are implicated in the development of hypertension through angiotensin II12–14 and central nervous system-mediated T-cell activation15 and vascular inflammation.1 Immune cell infiltration and their release of inflammatory cytokines like IL-1β have not only been associated with blood pressure elevation but also with end-organ damage associated with hypertension.16 Despite this evidence, the effect of therapies that specifically target inflammation on blood pressure is largely unknown. This evidence concerns the gene IL1B and Hypertension.