82, 106 Furthermore, overexpression of IL‐22 via exogenous administration of expressed IL‐22 via adenovirus or via targeted gene (i.e. transgenic mice for IL‐22) resulted in amelioration of liver fibrosis apparently due to senescence of b‐galactosidase‐positive HSCs.82, 106 In contrast, a single dose of IL‐22 via the expression of adenovirus induced CXCL1 in the liver attracting circulating neutrophils to cause acute inflammation.77 The gene discussed is IL22; the disease is Hepatic fibrosis.