Numerous studies have shown that osteoclast differentiation plays an important role in RA bone destruction.[29,30] In the present study, several DEGs of RA were enriched in osteoclast differentiation, such as FBJ murine osteosarcoma viral oncogene homolog, transcription factor family JUN (JUN), Jun B proto-oncogene, interleukin 1 receptor type 1 (IL1R1), suppressor of cytokine signaling 3, and transforming growth factor, beta receptor 2 (TGFBR2). The gene discussed is SOCS3; the disease is rheumatoid arthritis.