Several association studies in humans and experimental mouse models have hinted at the contributive role of the IL-17A pathway in the pathogenesis of SSC, showcasing increased IL-17A levels (or IL-23 as partner in crime) in serum and affected skin, as well as increased frequencies of IL-17A+-producing T cells(see Figure 2) [126, 129–133, 125, 134]. This evidence concerns the gene IL17A and systemic sclerosis.