However, NO secreted by AMs via inducible nitric oxide synthase (iNOS) may function as part of a physiological anti-apoptotic mechanism to prevent AECIIs from undergoing stretch-induced cell death (Edwards et al. 2000), as we recently showed that AECIIs damage was key to the progression of IPF (Yu et al. 2018) thus macrophages after stretching in IPF may attenuate the vicious cycles of AECIIs injuries. This evidence concerns the gene NOS2 and idiopathic pulmonary fibrosis.