This is consistent with the lower RANKL/OPG ratio that was observed when β-catenin was constitutively activated in non-CKD mice [36] and suggests that sclerostin, by inhibiting the Wnt/β-catenin pathway of osteoblast-lineage cells in CKD, could also lead to increased bone resorption on top of decreased formation. The gene discussed is TNFSF11; the disease is chronic kidney disease.