Previous studies also showed that Retnla induced myofibroblast differentiation and Retnla treatment inhibited tumor necrosis factor-α-induced activities of caspase-3 and caspase-8, indicating that Retnla might contribute to the pathogenesis of pulmonary fibrosis by induction of fibroblast resistance to apoptosis10,34. This evidence concerns the gene CASP8 and pulmonary fibrosis.