SAA is present in the blood of healthy individuals at low levels (20–50 mg/L), but its expression increases to about 1,000-fold within 24 h from the onset of acute phase response (APR), which includes a series of physiologic changes as a consequence of infection, inflammation, trauma, or other events (Gabay and Kushner, 1999; Yoo and Desiderio, 2003; Kushner, 1982). Here, SAA1 is linked to infection.