While much research on IPF has centered on redox imbalance, particularly focusing on signaling pathways involving NADPH oxidases, eosinophil peroxidase, mitochondrial electron transport chain, and myeloperoxidase, which can be activated to generate ROS [40,41], our study based on the expression of hypoxia signal in the IPF model, boldly demonstrated that the dynamic changes of redox imbalance, especially reductive stress, during the evolution of IPF disease could be monitored by PET imaging. This evidence concerns the gene MPO and idiopathic pulmonary fibrosis.