In particular, elevated MYB levels in T-ALL can arise either directly through TCR-mediated MYB proto-oncogene translocations, MYB duplications and enhanced TAL1 complex binding at the MYB locus or indirectly through the TAL1/miR-223/FBXW7 regulatory axis [125]. The gene discussed is MYB; the disease is acute lymphoblastic leukemia.