Hung et al. reported that CKD patients with secondary hyperparathyroidism increased expression of sclerostin that inhibits Wnt 10b/Wnt 16 signaling pathway, leading to activating osteoclastic bone resorption (tartrate-resistant acid phosphatase isoform 5b) and inactivating osteoblastic bone formation (procollagen type I propeptides), bone inflammation and low bone density, and ultimately adverse clinical events [25]. The gene discussed is SOST; the disease is secondary hyperparathyroidism.