To evaluate whether inhibition of TAK1 activation by resveratrol was responsible for attenuated inflammation and fibrosis in experimental pneumoconiosis, primary alveolar macrophages or lung fibroblasts isolated from silica-exposed rats were transfected with TAK1 overexpression vector or empty vector and then incubated with resveratrol or vehicle (DMSO) in vitro. The gene discussed is MAP3K7; the disease is pneumoconiosis.