Treatment with IL‐37 alleviated BLM‐mediated lung inflammation and fibrosis via the enhancement of autophagy and inhibition of TGF‐β1 receptor signaling in IPF fibroblasts, and administration of autophagy inhibitor 3‐methyladenine (3‐MA) could reverse this effect.[24] Surprisingly, there have been no reports with respect to the correlation between IL‐37 and tendon adhesion so far, and the functional role and underlying mechanisms of IL‐37 in tendon adhesion remain unknown. Here, IL37 is linked to idiopathic pulmonary fibrosis.