Confirming the importance of this interaction, the exogenous expression of c-Myc rescued the anti-growth and pro-apoptotic effects of Notch-inhibition by GSI in Notch-dependent T-ALL in vitro and in vivo [100], and consistently, it has been shown that T-ALL resistance to Notch-targeting agents is due at least in part by the chromatin modifier BRD4 that epigenetically sustains c-Myc expression and function [100,101,102]. The gene discussed is BRD4; the disease is acute lymphoblastic leukemia.