Akt1 enhanced mitophagy and induced the acquisition of apoptosis resistance in alveolar macrophages from IPF patients, thereby contributing to pulmonary fibrosis; conversely, impaired mitophagy induced by knockdown of Akt1 gene enhanced macrophage apoptosis and attenuated TGF-β1 activity, which spared mice from pulmonary fibrosis (Larson-Casey et al., 2016). Here, TGFB1 is linked to pulmonary fibrosis.