Putting our previous results into context, we learned that while there is a significant increase in the accumulation of autophagosomes (LC3β puncta) in IPF lungs compared to control non-IPF lung tissues (which shows dysregulation of autophagy flux in IPF lungs) (Figure 1I), the presence of LC3β puncta alone (Figure 2D), or when LC3β puncta are co-localized with UPR markers (Figure 3), is associated with improved lung function. This evidence concerns the gene MAP1LC3B and idiopathic pulmonary fibrosis.