Furthermore, in 5% of children with acute lymphoblastic leukemia (ALL), the t (1,19) chromosomal translocation specifically targets the E2A gene, resulting in an oncogenic E2A-PBX1 fusion protein and becoming a coactivator for RUNX1, resulting in unfavorable B-cell development [49]. The gene discussed is PBX1; the disease is acute lymphoblastic leukemia.