In the lungs of patients with pulmonary fibrosis (PF), miR-34a expression was significantly higher in the type II alveolar epithelial cells (AEC), and this may dysregulate cell senescence[38] and promote epithelial-mesenchymal transition.[39] In addition to overexpressed miR-34a, increased p53 acetylation and decreased SIRT1 have also been reported in AECs in PF. This evidence concerns the gene TP53 and pemphigus foliaceus.