An in vitro study suggested that GA might also act at the joint level on synoviocytes: the authors demonstrated that GA (0.1–1 μM) was able to counteract the proliferation of FLS from RA patients through pro-apoptotic mechanisms; moreover, it suppressed the expression of cytokines (IL-1β, IL-6), chemokines (MCP-1, MCP-3), MMP-9, and COX-2 versus the TNF-α challenge [42]. The gene discussed is IL1B; the disease is rheumatoid arthritis.