TAL1 and acute lymphoblastic leukemia: Studies of the pre-leukemic phenotype in mouse models suggest that both SCL and LMO2 overexpression causes T-ALL by inducing aberrant self-renewal of committed T-cells in the thymus, resulting in a cellular pool which can over time acquire additional gain-of-function mutations of genes involved in signalling pathways regulating T-cell development, such as NOTCH1, interleukin-7, KIT and FLT3 [20].