Although clinically and genetically heterogeneous diseases, T-ALL and AML present overlaps in genetic alterations that lead to pathogenic pathways, such as mutations in genes of the RAS signaling pathway (8), and cellular expression of lineage development markers, such as CD7 expression in AML and CD13 or CD33 in T-ALL (9). The gene discussed is ANPEP; the disease is acute lymphoblastic leukemia.