This hypothesis is further supported by the increased secretion of IL-1β and IL-18 in LPS-treated ATG16L1 or ATG7 knockout macrophages, as well as the increased susceptibility of ATG16L1 knockout mice to dextran sulfate sodium (DSS)-induced colitis, which could be ameliorated by the injection of IL-1β and IL-18 blocking antibodies [30]. The gene discussed is ATG16L1; the disease is colitis.