AKT3 and pulmonary fibrosis: Intriguingly, overexpression of miR-29a-3p was marked as an activator of protective autophagy by targeting Akt3/mTOR in transforming growth factor (TGF)-β-treated TC-1 cells, as a model of lung fibrosis, and resulted in amelioration of lung fibrosis and protection of lung epithelial cells [61].