Our hypothesis that tendon dysfunction could be justified in some patients by a glycol-lipid overload in fibroblasts would link with the evidence reflected in the study conducted by our group that shows evidence for such defective KCa3.1 regulation in Fabry disease fibroblasts and in Niemann-Pick C fibroblasts, disturbances in membrane trafficking, or function in the fibroblasts [23]. The gene discussed is KCNN4; the disease is Fabry disease.