In addition, chondrocytes, when stimulated with, e.g., IL-1β, TNF-α, or IFN-γ, show a classical RA-like phenotype as evidenced by decreased expressions of COL2 and aggrecan (ACAN) when MMP13 expression increases [80] and induced apoptosis in chondrocytes [81], reflecting the human in vivo situation [82,83]. The gene discussed is IL1B; the disease is rheumatoid arthritis.