Furthermore, we and others have identified the key role of mitochondrial dysfunction in the context of alveolar epithelial cell injury and apoptosis in pulmonary fibrosis that could be reduced by exogenous administration of the thyroid hormone and its analogues, leading to the resolution of lung fibrosis and inflammation in murine models, thus making it a potential therapeutic target [13,14,15]. This evidence concerns the gene TG and pulmonary fibrosis.