Among them, IL-21, IL-17A, and IFN-γ triggered the abnormal JAK/STAT signaling in the synovium, leading to joint destruction [118], while TNF-α activated the NF-κB pathway, enhancing TNFR-II expression and stimulating RANKL secretion in RA-FLS, thereby facilitating osteoclastogenesis [103]. The gene discussed is SOAT1; the disease is rheumatoid arthritis.