Mechanistically, they found that Hdac3 depletion leads to an increase in enrichment of H3K27ac decoration at the Runx3 and Gzmb (granzyme B) genomic loci, which was essential for CD8+ T cell cytotoxicity [55], whereas increased H3K27ac at Prdm1 (Blimp-1), which is a transcriptional repressor that enhances terminal differentiation of effector CD8+ T cells during viral infection [96], was necessary for T cell persistence during activation [55]. The gene discussed is CD8A; the disease is viral infectious disease.