Such complement activation may drive the immunopathology of FD at several levels: (i) through its impact on glucosphingolipid metabolism (56); (ii) cross-talk with Toll-like receptors (57, 58); and (iii) proinflammatory cytokine induction in the kidney (59), which could fuel profibrotic pathways induced by TGF-ß1, IL-6 and IL-10. The gene discussed is IL10; the disease is Fabry disease.