Although we can conclude that the enhanced IIo reactivity of old CD8+TM is in part controlled by their broader FasL induction, the precise mechanisms operative in this context remain to be elucidated and may involve accelerated virus clearance [9] through FasL-dependent cytolysis, nonapoptotic FasL:Fas interactions between CD8+TM and TN that facilitate concurrent Io CD8+TE differentiation [35], or perhaps the autocrine binding of secreted FasL that, akin to a mechanism proposed for tumor cells [36], may shield IIo CD8+TE from FasL-mediated fratricide. The gene discussed is CD8A; the disease is neoplasm.