In RA, persistent joint inflammation heightens osteoclast differentiation and activity while hindering osteoblast differentiation and function, resulting in an imbalance of bone homeostasis and subsequent bone degradation.[222] It has been demonstrated that countering IL‐1 with monoclonal antibodies or inhibiting soluble IL‐1 type II receptors can substantially mitigate cartilage and bone damage.[223] Fernandes et al. This evidence concerns the gene IL1B and rheumatoid arthritis.