It is thus reasonable to speculate that, mechanistically, the decrease in PQ-induced lung fibrosis in the lung-Cpr-null mice was due to a lowered ability to mediate PQ-induced redox cycling, and the resulting decreases in oxidative damage and subsequent proliferation of fibroblasts in nearby regions as an attempt to regenerate and restore normal architecture of the damaged tissue. The gene discussed is POR; the disease is pulmonary fibrosis.