DNA binding and transcriptional activity of P-S727-STAT3 probably require acetylation of K685 because (1) persistent acetylation of K685 on STAT3 has been observed in CLL cells, (2) acetylation of K685 promotes dimer formation, DNA binding and activation of transcription, and (3) K685 acetylation provides CLL cells with survival advantages [174]. This evidence concerns the gene STAT3 and B-cell chronic lymphocytic leukemia.