Also, the presence of cagA did not appear to be an important contributor to dyslipidemia, as indicated by the stronger correlations between plasma lipids and stomach H. pylori 16S than plasma lipids and artery or stomach cagA. This suggests that either local effects of H. pylori in the stomach or systemic effects of infection are responsible for plasma lipid alterations. This evidence concerns the gene S100A8 and metabolic syndrome.