Remarkably, mice lacking Atg7 in myeloid cells exhibited enhanced sterile lung inflammation, accompanied by submucosal thickening, goblet cell metaplasia, increased collagen content, heightened IL-1β, IL-18, and IL-17 levels in the lungs and serum and increased mortality following intraperitoneal LPS injection, while bleomycin administration aggravated pulmonary inflammation and induced severe fibrosis (Table 2, Supplementary Figure S1) [139]. The gene discussed is ATG7; the disease is inflammation.