The study of MHCI-dependent CD8+ T cell responses, however, have yielded ambiguous findings, with MHCI-deficient mice developing increased atherosclerosis [63] and Apoe−/− mice deficient in the transporter associated with antigen processing-1 (TAP-1), which is required for MHC class I antigen presentation, showing reduced CD8+ T cell levels but unaltered atherogenesis [64]. The gene discussed is CD8A; the disease is atherosclerosis.