The most common pediatric T-ALL translocation is t(5;14)(q35;q32), fusing a gene desert (a genomic region without protein-coding genes) downstream of BCL11B to TLX3 (20%–25% pediatric, 5% adult cases), or more rarely to NKX2-5 or ZEB2. 61Thereby, hijacking of BCL11B REs leads to overexpression of these translocation partners, which has been shown to be oncogenic.62 The gene discussed is BCL11B; the disease is acute lymphoblastic leukemia.