CDKN1A and idiopathic pulmonary fibrosis: Tissue homeostasis after miR‐30a and Exo inhalation was promoted through the clearance of dysfunctional mitochondria indicated by the downregulation of CytoC,[36] the promotion of myofibroblast and immune cell apoptosis through decreased BCL‐2 expression,[37] and deactivation of fibroblasts indicated by the downregulation of BAX.[38] IGF‐2, p21, and BID are upregulated in IPF and contribute to enhanced ECM deposition,[39] suppressed alveolar regeneration,[40] and alveolar epithelial cell apoptosis,[41] respectively.