Mullan et al. [43] have shown that pro-inflammatory responses of SAA closely correlate with SR-BI expression on RA FLCs (fibroblast-like cells) in vitro, and SAA-induced cytokine production in human microvascular endothelial cells can be down-regulated by SR-BI antagonists, ApoA-I mimetic peptides, and a specific anti–SR-B1 antibody. The gene discussed is APOA1; the disease is rheumatoid arthritis.