Within the inflammatory response, the Ang II/AT1 receptor-induced TNF-α signaling can control the generation of anti-inflammatory cytokine NO and potentiate renal expression of pro-inflammatory cytokines IL-1 and IL-6 through the activation of nuclear factor-κB (NF-κB) signaling, thereby functioning as a major regulator of inflammation and kidney damage [27, 28]. The gene discussed is IL1A; the disease is Nephropathy.