It has been proposed that the beneficial effect of PPARG activation in controlling lung fibrosis may be due to the receptor’s broad cellular distribution within the lung, as this is expressed by alveolar epithelial cells, fibroblasts, bronchial smooth muscle cells, type II pneumocytes, macrophages, endothelial cells, lymphocytes, and dendritic cells [177]. This evidence concerns the gene PPARG and pulmonary fibrosis.