Plasma cholesterol levels—particularly HDL-cholesterol—are rapidly reduced in severe sepsis, and HDL particle composition is altered to contain greater levels of pro-inflammatory serum amyloid A (SAA), and reduced apoA1, apoM and sphingosine-1-phosphate (S1P), thus impairing the cholesterol efflux and anti-inflammatory properties of HDL [38,58,59,60]. The gene discussed is APOA1; the disease is Sepsis.