Furthermore, mice exhibiting lung injury and fibrosis were detected in an animal model of silica-induced pulmonary fibrosis (PF), which alleviated the accumulation of inflammatory cells in bronchoalveolar lavage fluid in mice, and demonstrated that FA stopped the progression of PF and prevented epithelial-mesenchymal transition (EMT) in a dose-dependent manner by improving the expression of fibrotic proteins (including collagen I, TGF-β, p-smad2/3) [94]. The gene discussed is TGFB1; the disease is pemphigus foliaceus.