Therefore, the aberrant cell proliferation and increased survival of T-ALL are partly controlled by the Notch1-Myc transcriptional network.43 The Notch1-Hes1 regulatory axis is implicated in the upregulation of PI3K and NF-κB signaling as well as in the inhibition of apoptosis by repressing the proapoptotic BH3-only protein Puma.44 We could demonstrate that CJ was also able to downregulate the Notch1 target genes MYC and HES1, which may contribute to the induction of apoptosis. This evidence concerns the gene HES1 and acute lymphoblastic leukemia.