In a mouse model of the coxsackievirus B-induced pancreatitis, an overexpression of IL-17A and an expansion of the γδ T cells in the pancreas aggravated the inflammatory immunological injury to the pancreas, which was primarily induced via a pancreatic neutrophil infiltration and a peripheral Th17 response, and a γδ T-cell deficiency in a mouse model reduced the severity of pancreatitis (71). The gene discussed is IL17A; the disease is pancreatitis.