Then, the essential role of major histocompatibility complex class I (MHC-I) molecules in mediating CD8+ T-cell-dependent anti-malarial immunity was shown by the study in which adoptive transfer of malaria-immune splenocytes into β2 microglobulin (β2 m)-deficient mice failed to confer protection (White et al., 1996). The gene discussed is CD8A; the disease is malaria.