By assessing the expressions of p22phox, p40phox and p-p47phox subunits in silica-induced pulmonary fibrosis, we proved that activation of the NOX2 may be attributed to the phosphorylation of p47phox, supporting the importance of NOX-derived ROS in the pathogenesis of silicosis. The gene discussed is NCF4; the disease is pulmonary fibrosis.