This evidence suggests a reciprocal model whereby TNF-α produced by immune cells inhibits endothelial and epithelial function and, in the injured renal parenchyma, can further potentiate inflammation via autocrine TNF-α signaling, perhaps creating a loop towards sterile inflammation, vascular injury, and fibrosis associated with hypertension-related nephropathy. The gene discussed is TNF; the disease is Hypertension.