Therefore, the presence of notable percentages of NKT cells up to eight months post infection may, on the one hand, support the evidence that the inflammatory trigger (i.e., likely some inactive viral remnants) is not fully cleared, but on the other hand, may also indicate an NKT cell-mediated cytotoxic activation that is still alert and probably compensates the role of the restored to-nearly-normal levels NK and CD8+ T cells. The gene discussed is CD8A; the disease is infection.