We hypothesize that the inflammatory cytokines, including TNF-α, IL-6 and IL-1β, known to be elevated in patients with HTN, likely induce the expression of pathogenic APOL1 via JAK-STAT signaling, thereby contributing to the pathogenesis of APOL1-mediated, HTN-CKD.23, 24, 25, 26 Therefore, we hypothesize that clinically available inhibitors of JAK1/2 will block kidney APOL1 expression and thereby slow the progression of APOL1-mediated HTN-CKD. The gene discussed is JAK1; the disease is hypertensive disorder.