This stems from the fact that c-myc oncoprotein occupies 15% of the total genome promoters and plays a heavy role in many contexts of tumorigenesis including cell cycle, differentiation, proliferation, and metabolism.1 The significance of c-myc deregulation is documented in T cell acute lymphoblastic leukemia, multiple myeloma, and certain subsets of Burkitt’s lymphoma.2 Its involvement in such aggressive malignancies suggests that therapeutic efforts aimed at inhibiting MYC expression or activity should have an important clinical relevance. Here, MYC is linked to T-cell acute lymphoblastic leukemia.