Regarding the H. pylori-atherosclerosis association, some possible explanations consider, (a) the bacterial direct action over the arterial walls, (b) indirect induction of endothelial damage by the gastric inflammatory process, (c) cross-reaction between antibodies against the CagA antigen with epitopes on the arterial walls, (d) induction of hypercholesterolemia by inhibition of LDL capture, and (e) foam cell formation by regulation of the reverse cholesterol transport. This evidence concerns the gene S100A8 and familial hypercholesterolemia.