Mice with a conditional deletion of Blimp1 in CD8+ T cells, mediated by crossing Prdm1F/F mice with mice expressing CRE recombinase under human Granzyme B promoter control (GzBCRE), exhibit increased numbers of antigen-specific CD8+ effector cells after infection but stunted terminal effector differentiation, and Blimp1 was shown to mediate downregulation of IL-2 and control of effector responses and proliferation in CD8+ cells, further establishing the importance of Blimp1 in preventing unrestrained inflammatory responses to infection (33). The gene discussed is PRDM1; the disease is infection.