Fibrosis in BA is enhanced by proinflammatory cytokines, mainly interferon gamma (IFN-γ), which promote HSC proliferation and secretion of fibrotic factors, including MMPs, tissue inhibitors of metalloproteinases (TIMPs), and collagen regulatory T cells (Tregs) inhibit T helper 1 (Th1) and/or IFN-γ-induced effects on HSCs by suppressing Th1-induced activation of signal transducer and activator of transcription 1 (STAT1). The gene discussed is IFNG; the disease is fibrosis.