LMO2 and acute lymphoblastic leukemia: The redundancy of LMO gene family members is analogous to the findings in the TAL1-overexpressing subtype of T-ALL, in which LMO1 or LMO3 can be aberrantly activated by chromosomal translocation and substitute for LMO2 in the TAL1 CRC that drives thymocyte transformation (54–56).