Activation of cell surface receptors for SAA such as receptor for advanced glycation end products (RAGE), toll-like receptor (TLR) and formyl peptide receptor-like 1 (FPRL-1) also stimulate NFκB activation [22] and inhibition of these receptors, or SAA activity, can ameliorate SAA-mediated endothelial dysfunction [26]. The gene discussed is FPR2; the disease is endothelial dysfunction.