Proinflammatory cytokines such as IL-1β and tumour necrosis factor alpha influence the expression of cathepsin K. Its overexpression in the rheumatoid synovium, induced by IL-1β and tumour necrosis factor alpha due to the increase of cathepsin K-expressing cells, proves this protease to be a valuable tool for bone research, and cathepsin K also may become a new and highly specific biomarker for RA [26]. This evidence concerns the gene IL1B and rheumatoid arthritis.