Helicobacter pylori infection, which is associated with gastric inflammation, ulcers, and cancer, is additionally mediated by interactions between membrane cholesterol and the virulence protein cytotoxin-associated gene A (CagA), whereas cellular cholesterol depletion by methyl-β-cyclodextrin (MβCD) or lovastatin was shown to reduce CagA translocation and pro-inflammatory interleukin 8 (IL-8) secretion in human gastric adenocarcinoma AGS cells [43,44]. The gene discussed is S100A8; the disease is ulcer disease.