HIV infection, for example, induces high levels of virus‐specific CD8+ T cell activation, which is much reduced in elite controllers, but there is also a great deal of evidence that CD8+ T cells can contribute to protection against progression.70 Thus, MAIT cell activation may be—like many effector responses—a two‐edged sword, with the overall outcome dependent on the dose and timing of infection, and the presence of other effector responses. The gene discussed is CD8A; the disease is HIV infectious disease.