As an agonistic ligand for Notch receptors, DLL1 is overexpressed in AML with poor prognosis (Additional file 1: Fig. S12A, B) and triggers proteolytic cleavage of Notch receptors, and the resulting Notch intracellular domain can be translocated into the nucleus and interacted with CSL to activate the transcription of target genes, such as CCND1, HES1 and MYC, which in turn promotes tumor cell proliferation and survival [40, 41]. The gene discussed is HES1; the disease is acute myeloid leukemia.