TAL1 and B-cell chronic lymphocytic leukemia: A paradigmatic example is the hotspot for insertions that create a de novo super-enhancer upstream of TAL1, leading to its overexpression in roughly 5% of pediatric T-ALLs.287 In contrast, an enhancer located 330 kb away from PAX5 is disrupted by somatic mutations in 8% cases of chronic lymphocytic leukemia (CLL), 29% of diffuse large B-cell lymphoma (DLBCL) and 5% of mantle cell lymphoma (MCL).288