demonstrated that lack of ABCA1 and ABCG1 on macrophages augments the inflammatory response with enhanced expression of TLR4 on the cell surface due to increased retention of membrane cholesterol.5 Furthermore, Zhu and colleagues have previously shown that myeloid deficiency of ABCA1 protects mice against Listeria monocytogenes infection.13 It is therefore plausible that under a classically inflamed environment, downregulation of ABCA1 could be beneficial to help propagate the inflammatory response. This evidence concerns the gene ABCG1 and listeriosis.