Several transcription factors are known to modulate effector function (blue), exhaustion (red), and memory phenotype (light green) in T cells. Yoshikawa et al clearly establish PRDM1 as a repressor of memory function in antitumor T cells. PRDM1 deletion resulted in upregulation of TOX and EOMES in T cells. EOMES upregulation in PRDM1-deficient T cells partially explains the promotion of memory phenotype. However, upregulation of TOX in PRDM1-deficient T cells further raises interesting questions regarding epigenetic programs linking memory and exhaustion.