In the TAA-induced ALI mouse model, rCHI3L1 inhibits the differentiation of IFN-γ+ Th1 cells through the STAT3 signaling pathway, thereby suppressing IFN-γ secretion and improving Th1 cell-mediated inflammatory response in the liver, providing a possible target for ALI treatment [98,99]. The gene discussed is IFNG; the disease is acute respiratory distress syndrome.