It seems reasonable to target TGF-β during acute sepsis because the anti-inflammatory and immunoregulatory effects of TGF-β involve activation of Smad7, and inhibition of renal inflammation is associated with marked upregulation of renal Smad7 and suppression of NF-κB activation to switch off the inflammatory response [23, 24]. The gene discussed is TGFB1; the disease is Sepsis.