The genetic manipulation of ApoA1 expression in septic mice showed that its deficiency strongly increased inflammatory cytokine production, while ApoA1 overexpression in septic mice, or their treatment with HDL or with ApoA1 mimetic peptides, reduced inflammation and protected them from sepsis, at least in part, through neutralization of bacterial endotoxins [131,132,138,139,140]. The gene discussed is APOA1; the disease is Sepsis.