For example, one subtype of T cell acute lymphoblastic leukemia (T-ALL) arises from somatic mutations at noncoding sites upstream of the TAL1 gene in which a binding site of transcription factor MYB is imported, thus forming an SE and, finally, resulting in the overexpression of TAL1 (Mansour et al., 2014). Here, TAL1 is linked to T-cell acute lymphoblastic leukemia.