Use of these data can help establish a regulatory mechanism for hereditary risk of high hyperdiploidy ALL, a hypothesis put forth by the consortium to evaluate a risk allele within the enhancer element on chromosome 10p21.2 that disrupts RUNX3 binding, decreases ARID5B expression, and arrests normal lymphocyte development to initiate leukemogenesis76. The gene discussed is RUNX3; the disease is acute lymphoblastic leukemia.