The expression of BEX1 and BEX2 has been previously shown to be regulated by epigenetic mechanisms including promoter methylation.47 Both BEX1 and BEX2 have been described as tumor suppressor genes in glioma47 and acute myeloid leukemia (AML).48, 49 However, the function and prognostic relevance of these genes in T‐ALL biology remain to be evaluated. The gene discussed is BEX1; the disease is neoplasm.