In RA patients, the levels of pro-inflammatory cytokines, such as TNF-α and IL-6, are significantly elevated, inducing an increase in the expression of RANKL in peripheral blood mononuclear cells (PBMC) (16), and the high expression of RANKL drives the generation of a large number of highly activated OC, which increases bone resorption, and is the core driver of the imbalance of bone metabolism and bone destruction in RA patients (17). This evidence concerns the gene IL6 and rheumatoid arthritis.