The fact that these genomic variations have been found heterozygous in a subset of T-ALL cases [2] and moreover that this is not the only genomic background or epigenomic mechanism linked to TAL1 overexpression in T-ALL (e.g., TAL1d 90-kb deletion) [102] illuminates the perplexing nature of pathways that are followed during tumorigenesis. The gene discussed is TAL1; the disease is acute lymphoblastic leukemia.