BIRC3 and idiopathic pulmonary fibrosis: The miR‐30a and Exo may interact in the lung to both reduce alveolar epithelial cell loss and induce myofibroblast de‐differentiation.[34] Prior research showed apoptotic‐resistant fibroblasts are accumulated in IPF and inhibition of IAP proteins enhances myofibroblast apoptosis in a bleomycin model of IPF.[35] Both miR‐30a and Exo treatments significantly reduced cIAP‐2 expression in pulmonary tissue.