Increasing evidence has recently indicated that sepsis patients and animal models of sepsis exhibit reduced ATG5/ATG16L1 expression and autophagic activity in the late stage of sepsis and this lagging suppression of autophagic activity may contribute to inflammatory dysregulation, mitochondrial dysfunction and apoptosis, which are strongly correlated with organ dysfunction and mortality following sepsis37–40. The gene discussed is ATG16L1; the disease is Sepsis.