A study showed that among TAO patients, circulating CXCL10 levels (sCXCL10) were significantly higher in active TAO than those in inactive disease, and stimulation with IFN-γ or TNF-α plus IFN-γ induced CXCL10 release, while CXCL10 production was absent under basal conditions in primary cultures of retrobulbar fibroblasts and retrobulbar preadipocytes from TAO patients, which suggested that fibroblasts or preadipocytes could participate in the pathogenesis of TAO by chemokines [140]. This evidence concerns the gene TNF and thromboangiitis obliterans.