Wnt1 mutations cause osteogenesis imperfecta in humans [35, 36], osteoblastic Wnt5a regulates osteoclastogenesis [37] at least in part through interaction with Wnt16 [38], overexpression of Wnt7b in osteoblasts dramatically increases bone mass [39], and Wnt4 overexpression in osteoblasts prevents bone loss associated with ovariectomy or ageing [40]. The gene discussed is WNT16; the disease is osteogenesis imperfecta.