These data in the Sirt3Tg mice suggest that SIRT3 overexpression attenuates lung Mo-AM recruitment following asbestos exposure and add to the accumulating evidence implicating Mo-AMs in the pathobiology of pulmonary fibrosis in mice as well as in humans with IPF [40,41,42,55,56,57,58]. Here, SIRT3 is linked to idiopathic pulmonary fibrosis.