Our preliminary data suggest that HCV infection of thyrocytes, as well as of beta cells, may upregulate CXCL10 gene expression and secretion (as shown in human hepatocytes); the consequent recruitment of Th1 lymphocytes that secrete IFN-γ and TNF-α may in turn induce CXCL10 secretion by infected cells, thus perpetuating the immune cascade responsible for these endocrine disorders. The gene discussed is CXCL10; the disease is endocrine system disorder.