They proposed two mechanisms by which SIRT-3 exerts its anti-fibrotic effect in mouse models of asbestos-induced pulmonary fibrosis: prevention of mitochondrial DNA damage and subsequent apoptosis of alveolar epithelial cells, as well as inhibition of macrophages recruitment from monocytes into the alveoli following exposure to asbestos Similarly, Rehan et al. found reduced levels of SIRT-3 in lung biopsies from patients with IPF [22]. The gene discussed is SIRT3; the disease is idiopathic interstitial pneumonia.