Its role in the prevention and management of RA is not fully understood; however, preclinical evidence showed that this compound could positively affect RA via the reduced expression of β3 integrin, cathepsin K [208] and RANKL [209,210], reduce the number of Th17 cells [211], suppress MAPK or the NF-κB pathway, and alleviate bone degradation in the rodent models of CIA [212,213]. The gene discussed is CTSK; the disease is rheumatoid arthritis.