Thus, a combination of events that significantly reduce RA-FLS apoptosis results from the elevated levels of several pro-inflammatory cytokines (e.g., TNF-α, IL-1ß, IL-6, IL-7, IL-8, IL-12/IL-23, IL-15, IL-17, IL-18, IL-32, IFN-γ] and growth factors, including fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), which cause an aberrant survival of RA-FLS [3,30,31,32,33,34,35]. This evidence concerns the gene IL17A and rheumatoid arthritis.