We found that whereas repeated administration of both poly(I:C) and saline control to MRL/MpJ mice led, as expected, to the development of AIP characterized histologically by destruction of pancreatic acinar architecture, infiltration of immune cells, and massive fibrosis, repeated injections of both poly(I:C) and the inhibitor of TLR3 signaling led to only minor histologic changes of this kind (Figure 1, A and B). This evidence concerns the gene TLR3 and autoimmune pancreatitis.