TAL1 and acute lymphoblastic leukemia: Our discovery of an aberrant oncogenic enhancer upstream of the LMO1 gene differs in important ways from the super-enhancer we identified upstream of the TAL1 gene.5 Although enhancer mutations in both cases create a de novo MYB binding site, which in turn initiates a large aberrant enhancer that drives expression of a T-ALL oncogene, the mutations upstream of TAL1 consist of 2- to 18-bp insertions, while in the case of LMO1, the causal mutation is a C-to-T single nucleotide transition.