Notably, CXCL10 is highly expressed in SFs of aggressive RA cases [102], and its elevated levels stimulate Th1-directed T cells, leading to IFNγ and TNF-α production and triggering CXCL10 secretion from various cells, thereby perpetuating an amplifying feedback loop that sustains the autoimmune process [103]. The gene discussed is IFNG; the disease is rheumatoid arthritis.