TNFSF11 and Fabry disease: Finally, the multiple mouse models of FD [73, 74] have supported observational hypotheses, helped to unravel the pathophysiology of FD, and led to multiple novel molecular observations, including: preclinical support for RANKL blockade as a treatment for FD [29], a pathogenic role for brain-derived neurotrophic factor in FD [32], different age- lesion- and histology-related molecular profiles of FD lesions [52], and a potential role of Wnt/β-catenin signaling in FD [13].