RA can induce an imbalance between autophagy and mitophagy, leading to the secretion of proinflammatory factors and RANKL in fibroblast-like synovial cells, which mediates the activation of bone resorption, destroys the balance of bone turnover, promotes more active osteoclasts and aggravates osteoporosis, osteolysis, and connective tissue damage [15–17]. This evidence concerns the gene TNFSF11 and rheumatoid arthritis.