Although further studies are needed to fully elucidate the interaction between IL-31 and TGF-β1 in the pathogenesis of SSc, one possibility is that IL-31RA expression in SSc patients and BLM model is already elevated (Figs. 2, 5f) and the further up-regulation by anti-TGF-β1 antibody does not necessarily lead to the enhanced signaling through the IL-31/IL-31RA axis. This evidence concerns the gene TGFB1 and systemic sclerosis.