Considering that in thyroid tissues, recruited Th-1 lymphocytes are responsible for enhanced IFN-γ and TNF-α production, which in turn stimulates CXCL10 secretion in thyroid cells perpetuating the autoimmune process [93], thus TNF-α stimulation of thyrocytes would clarify whether inflammatory microenvironment upregulates CXCR3 expression promoting thyroid tumorigenesis. The gene discussed is CXCR3; the disease is thyroiditis.