HDAC1 and hematopoietic and lymphoid system neoplasm: The present study showed that BSO downregulated in JK cells, as an experimental model of blood, and in HeLa and MCF7 cells, as examples of solid malignancies, had the expression of both DNMT1and HDAC1, which are well known partners of UHRF1 [31], suggesting that the use of TQ-rich BSO represents a promising strategy for epigenetic therapy for both solid and blood tumors through direct targeting of UHRF1 and/or its partners DNMT1 and HDAC1.