The importance of the anti-inflammatory role of autophagy has been demonstrated in vivo, since Atg16L1 deficiency increased the production of IL-1β and IL-18 in a model of chemically induced colitis in mice [63] and in mouse models of sepsis where lack of autophagy caused more susceptibility to endotoxemia with increased IL-1β and IL-18 serum levels [76]. This evidence concerns the gene IL1B and serum lipopolysaccharide activity.