Consistent with this idea, Mueller and Ahmed observed that decreasing MHC Class I stimulation of CD8 T cells (with an MHC I −/− environment using bone marrow chimeric mice) resulted in increased numbers of polyfunctional T cells during a persistent LCMV Clone 13 infection [61] (polyfunctionality referring to the extensive production of multiple cytokines by an individual T Cell, a paradigm established in part by LCMV). The gene discussed is CD8A; the disease is infection.