Whereas in human samples, the levels of RUNX2 positivity within FD lesions were highly variable before and after denosumab treatment, mouse studies have helped clarify the differentiation status of BMSCs in FD lesions, revealing a significant decrease in RUNX2-expressing FD cells in αRANKL-treated mice (Fig. 4d), together with a reduction in the early to mid-osteogenic differentiation marker ALP (Fig. 4c). The gene discussed is RUNX2; the disease is Fabry disease.