The overexpression of receptor interacting serine/threonine kinase 3 (RIPK3) and mixed lineage kinase-like (MLKL) was detected in AT2 of SFTPA1 homozygous knockout mice, but both RIPK3 and MLKL could significantly improve the progression of IPF, suggesting that the SFTPA1 homozygous mutant reduced SP-A production. The gene discussed is RIPK3; the disease is idiopathic pulmonary fibrosis.