Several studies have proposed in Systemic sclerosis (SSc) patients that the monokine induced by interferon (IFN)-γ(MIG)/chemokine receptor (CXCR)3 axis has a determinant role in the autoimmune process and in fibrosis. Elevated MIG levels were linked to a more severe clinical phenotype, with kidney, lung and thyroid involvement. Then MIG could be considered a marker of a more aggressive autoimmune process. In vitro, SSc fibroblasts have different kinds of dysregulation in the secretion of MIG, once treated with cytokines (as interferons). Moreover, MIG has been suggested as a serologic marker of a more severe SSc form, so it could be useful for the risk stratification of SSc patients.