AXIN1 and Fabry disease: Non-mutational β-catenin accumulation may be mediated by different indirect mechanisms, for instance PDGF receptor activation [39], plakoglobin loss [40], epigenetic WNT inhibitor inactivation [41], parathyroid hormone action [42], and by constitutive activation of Gα proteins exerting their effects in modulating the WNT/β-catenin pathway competing for axin, therefore acting on the axin-containing β-catenin destruction complex, as recently showed by Regard JB in FD [43].