In addition, BTZ successfully modulated the oncogenic T-ALL driver NOTCH1 by suppressing the expression of Notch and its target genes (HES1, GATA3, and RUNX3) in parallel to a synergistic activity with dexamethasone, leading to a near-complete remission of T-ALL xenografted tumors in vivo (Bassan et al., 2018[10]). Here, HES1 is linked to acute lymphoblastic leukemia.