Its role in the pathogenesis of B-ALL is based on the regulation of gene expression: FOXO1A (bone marrow cell differentiation, higher risk of relapse in ALL), MS4A1 (encoding B-lymphocyte marker—CD20) and PBX1 (involved in ALL pathogenesis, unfavorable prognosis, association with hyperleukocytosis) [80,81,82,83]. This evidence concerns the gene PBX1 and acute lymphoblastic leukemia.