Taken together, our data and data from previous studies from independent groups (6, 7) suggest that T cell response in SSc might be also aimed to contrast aberrant TGF-β-dependent myofibroblast activation that is seen in this disease and that IL-17A might play a prominent dual role in this scenario (10–14), bridging a T cell response from a protective role to a profibrotic one in the long term. The gene discussed is TGFB1; the disease is systemic sclerosis.