Furthermore, Gerby et al. [8] also showed that Myc acts as a critical mediator of pre-LSC activity downstream of Notch1, suggesting that combined NOTCH/MYC inhibition by γ-secretase and BET-bromodomain inhibitors [11] could further potentiate therapeutic targeting of the pre-LSC population in the context of human T-ALL (Fig. 1). Here, MYC is linked to acute lymphoblastic leukemia.