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 hypertensive disorder.