The potential for TNF-α antagonism to reduce proteinuria in resistant FSGS is based on the finding of elevated TNF-α levels in experimental models of the disease and in patients with FSGS, induction of proteinuria in animals by TNF-α from mononuclear cells taken from patients with FSGS, and reduction in proteinuria with a TNF-α antagonist in the angiotensin II-induced renal injury model and other models that resemble FSGS [22]. The gene discussed is AGT; the disease is focal segmental glomerulosclerosis.