LMO2 and acute lymphoblastic leukemia: Although none of the variants found have been specifically described to have a causal role in tumor formation, it could be possible that they might have influenced the timing and function of the targeted genes, predisposing for the T-ALL development through various mechanisms (tumor intrinsic and/or immune-mediated) and in combination with the LMO2-activating insertion and the multiple acquired somatic alterations occurring in the tumor cells.