Together with the finding that ASXL1N646 retains BAP1 binding but loses interaction with at least nine additional DNA-binding transcription regulators beside FOXK1/K2, it raises a possibility that the interference with BAP1-ASXL1-TF axis may represent a mechanism for C-terminally truncated mutant ASXL1 to regulate target genes and leukemia cell growth. This evidence concerns the gene TF and leukemia.