As shown in Figures 3A, B, activation of Beclin-1 by forced expression of Becn1F121A/F121A or by TB-peptide provided similar levels of substantial reduction in circulating cytokines, as well as in pulmonary cytokines, indicating that Beclin-1–dependent autophagy provides anti-inflammatory effects during sepsis. The gene discussed is BECN1; the disease is tuberculosis.