RA-FLSs can be activated by the stimulation of cytokines such as IL-38, which induce the expression of pro-inflammatory cytokines (IL-6 and TNF-α) and angiogenic factors (vascular endothelial growth factor [VEGF] and HIF-1α) (164) that control RA-FLS proliferation and apoptosis in a concentration-dependent manner. This evidence concerns the gene VEGFA and rheumatoid arthritis.