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). This evidence concerns the gene LMO1 and acute lymphoblastic leukemia.