In contrast, findings from a mouse model of X-linked hypophosphatemia of this condition, characterized by a deficiency in the Wnt coreceptor LRP6 (low-density lipoprotein receptor-related protein 6) and the subsequent reduction in Wnt signaling, showed no alteration in FGF23-induced phosphaturia or deficits in bone mineralization, suggesting a different Wnt pathway involved in phosphate homeostasis [79]. Here, LRP6 is linked to X-linked hypophosphatemia.