A role for mitochondrial ROS is also supported by our recent study showing that diminishing AEC mitochondrial ROS production using MCAT mice that globally overexpress mitochondria-targeted human catalase reduces mtDNA damage in the setting of oxidative stress and subsequent AEC apoptosis and lung fibrosis following exposure to either asbestos or bleomycin [6]. The gene discussed is CAT; the disease is pulmonary fibrosis.