EFNB1 has been identified among downregulated DEGs in children diagnosed with AML [134], while bone marrow samples from pediatric AML patients are characterized by EPHB1 promoter hypermethylation with subsequent decreased EPHB1 expression [136], while analogously for the case of pediatric ALL, the observed increased EPHB4 methylation resulting in decreased EPHB4 expression may contribute to leukemia development and progression [131]. The gene discussed is EPHB4; the disease is acute myeloid leukemia.