Consistent with this notion, we observed the upregulation of the signalling pathways previously associated with SSc,3 33 such as interleukin (IL)-6, IL-4, IL-17, IL-1β, toll-like receptor, vascular endothelial growth factor (VEGF) signalling, JAK-STAT signalling as well as pathways involved in wound healing and extracellular matrix organisation (online supplemental figure S11C). The gene discussed is SOAT1; the disease is systemic sclerosis.