In this regard, our study found that WNT1 c.110G>T and c.505G>T mutations inhibited the cell viability, weakened the mRNA and protein expression levels of BMP2, and enhanced the mRNA and protein expression levels of RANKL, indicating that WNT1 c.110G>T and c.505G>T mutations can lead to osteoblast phenotype dysplasia, inhibit bone formation, and easily lead to an increased risk of osteoporosis and fracture. The gene discussed is TNFSF11; the disease is osteoporosis.