In the trinitrobenzene sulfonic acid (TNBS) induced-pancreatitis rat model, administration of anti-CXCL9 antibody worsened fibrosis, whereas administration of recombinant CXCL9 improved fibrosis, as assessed by trichrome staining and hydroxyproline assay61 (Table 1).In vitro stimulation of pancreatic stellate cells with CXCL9 downregulated TGFβ1 and col1a1 production by confocal microscopy. The gene discussed is CXCL9; the disease is pancreatitis.