First, we hypothesized that apolipoprotein B (ApoB), the major structural protein of very low-density (VLDL) and low-density lipoproteins (LDL), contributes to the resistance of C57BL/6 mice to S. aureus in our infection model, because the gene encoding Apo B (Apob) was expressed to a greater extent in the kidneys of C57BL/6 than in the kidneys of A/J mice at both gene expression (Fig. 5a) and protein level (Fig. 5b), before and after infection (Fig. 5c). The gene discussed is APOB; the disease is infection.