Sepsis induces significantly increased plasma TNF-α, creatinine and causes tubular damage and multiple organ injury, sepsis also induces increased mRNA for TNF-α, tissue factor, PAI-1, and urokinase-like plasminogen activator; all of these changes can be significantly decreased by EP treatment (a single dose of 40 mg/kg was intraperitoneally injected 12 h after cecal puncture and experiment finished 24 h after cecal puncture), therefore, EP attenuates sepsis-induced ARF in an animal model [68]. The gene discussed is TNF; the disease is acute kidney injury.