The authors observed that selenium, at supraphysiologic and nontoxic doses, induced selective ATM-p53-dependent apoptosis and higher intracellular oxidative stress (or levels of ROS) in chronic or acute myeloid leukemia stem cells among two established leukemia murine models and in AML or blast-crisis CML patient samples. This evidence concerns the gene TP53 and acute myeloid leukemia.