However, our present findings also uncovered that TBX21 is not the “driver” but rather a marker of tg-STAT6-enhanced chemosensitization of ALL cells to Ara-C, although the knockout or downregulation of STAT6 can considerably lead to an increase of Ara-C-induced transcription of TBX21. Regarding the relevance of the possible linkage of TBX21 (or T-bet) to Ara-C chemosensitization, whether STAT6 can exert noncanonical transcriptional inhibition on TBX21, warrants further studies. This evidence concerns the gene STAT6 and acute lymphoblastic leukemia.