Most likely through reduced transcription at BRD4-regulated loci and/or chromatin reorganization, BET-i reduces expression of exhaustion-associated genes, curtailing IR expression and relieving TCF1 suppression by other TFs (e.g., T-BET, BATF) to promote a more progenitor-like T cell phenotype in CLL patient T cells. This evidence concerns the gene BATF and B-cell chronic lymphocytic leukemia.