The serum amyloid A family of proteins is encoded by multiple genes, and it shows a high degree of homology in mammals. The human genome includes four SAA genes: SAA1 and SAA2, which are acute-phase proteins, SAA3 is a pseudogene (while the murine homolog codes for SAA3 protein), and SAA4 is a constitutively expressed protein. SAA1 is a non-glycosylated acute-phase protein, which can increase up to 1000-fold during inflammation. High levels of SAA1 and SAA2 correlate with the severity of inflammatory diseases such as atherosclerosis, rheumatoid arthritis, and cancer. SAA binds to the G protein-coupled formyl peptide receptor 2 (FPR2). Additionally, SAA stimulates G-CSF production through TLR2, leading to neutrophilia. Also, SAA binding to TLR2 results in NF-κB activation and enhanced expression of proinflammatory and anti-apoptotic genes. Thus SAA contributes to the inflammatory process. SAA1 in plasma is associated with high density lipoproteins (HDL), and modulates the atheroprotective properties of HDL during inflammation.