Although the timing of upregulation of type I and II IFNs during ILD, as well as their role(s) as primary versus secondary drivers of disease is not precisely known, and may vary between IPF and SSc-ILD, ultimately the upregulation of both IFN-γ and Type I IFN signaling may be detrimental in human lung fibrosis. This evidence concerns the gene IFNG and systemic sclerosis.