The present data demonstrates that increased circulating IL-13 may be associated with ventilation function impairment, which supports our theory that IL-13 plays a role in the pathogenesis of lung inflammatory and alveolar remodeling in pneumonoconiosis and provides evidence that Th2 cell polarization involving IL-13 may favor the development of pulmonary fibrosis [12,14,37]. The gene discussed is IL13; the disease is pulmonary fibrosis.