The pattern of IFN gene expression, lacking CXCL9, which is highly regulated by IFN-γ in vitro (48), makes it more likely these genes are responding to type I IFNs, either IFN-β from fibroblasts or IFN-α possibly from plasmacytoid DCs upregulated in SSc skin (49). The gene discussed is IFNG; the disease is systemic sclerosis.