Prior to the development of mice carrying the causative GNAS variants, some features of FD pathology could be replicated with close approximation in mice with receptor-dependent abnormal activation of the Gαs signaling pathway in osteoblasts (Col1-caPPR [66] and Col1(2.3)/Rs1 mice [67]) and in Osx-Cre; CatnbEx3/+ mice characterized by enhanced Wnt/β-catenin activity in osteoprogenitor cells [68]. This evidence concerns the gene GNAS and Fabry disease.