Treatment with this agent increased the levels of intracellular miR-29b by around 600-fold and led to the downregulation of the DNA methyltransferase 1 (DNMT1), DNA methyltransferase 3 alpha (DNMT3A), and Sp1 transcription factor (SP1) in cancer cells, thus reducing CLL’s selective hypermethylation and restoring mechanisms of apoptosis. Here, SP1 is linked to B-cell chronic lymphocytic leukemia.