Furthermore, in light of a prior study showing that restimulated CD8+ T cells FACS-isolated 30 days after LCMV-Cl13 infection exhibited a reduced capacity to undergo asymmetric cell division [32], which has been shown to result in differentially fated progeny during acute infection [26,33], it is intriguing to speculate that formation of the transcriptionally homogenous Div1CL13 population may result, in part, from an impaired capability to undergo asymmetric division. The gene discussed is CD8A; the disease is infection.