Acute lymphoblastic leukemia (ALL) is a malignant disorder that originates from one singlehematopoietic precursor committed to the B- or T-cell lineage1. ALL represents a biologicallyand clinically heterogeneous group of B/T-precursor-stage lymphoid cell malignancies arisingfrom genetic insults that block lymphoid differentiation and drive aberrant cell proliferationand survival2.As a consequence there is accumulation of an immature B- or T cell clone in the bone marrowresulting in the suppression of normal hematopoiesis and in various extra-medullary sites. 80-85% of ALL are B-cell lineage (B-cell precursor ALL), and 15-20% are T-cell lineage (TALL). Normal lymphocyte ontogeny takes place in the central lymphoid organ: in the bonemarrow for B-cells and in the thymus for T-cells. During the maturation process, specific cellsurface receptors are triggered to initiate a program of a sequential gene expression thatcommits developing cells to a B- or T-cells fate, drives the proliferation of progenitors andinitiates the rearrangement of antigen receptor genes. The acquisition and expression of amature and unique antigen receptor is a central feature of both B- and T-cell maturation andvery similar molecular and cellular events characterize the early development of B- and Tcells1.Incidence and cure rates differ among children and adults. In children, ALL is the commonestmalignancy accounting for approximately 25% of childhood cancer; in adults, this disease isless common and generally carries a worse prognosis. Although there is a remarkableprogress made in the treatment of ALL in children and, with less efficacy in adults, severalALL subtypes continue to have a poor prognosis.Consequently there is the need to improve the molecular dissection of subtypes, identifyingthe genetic alterations that predict the risk of treatment failure, and developing novel andtargeted therapies2