Furthermore, recent evidence suggests macrophages originating in the spleen, where GPR35 is highly expressed,2 may contribute to Ang II–induced cardiac fibrosis and hypertension.34 A role for GPR35 in the prohypertensive immune response is an interesting possibility that has not previously been explored, and future studies into the effects of GPR35 on markers of vascular inflammation and release of immune cells from the spleen in models of hypertension could yield further insight. The gene discussed is AGT; the disease is hypertensive disorder.