In this study, we could demonstrate that ATO at doses below the clinically achieved plasma levels of current ATO-containing treatment regimens in APL [30] displayed significant growth-inhibitory and cytotoxic activity preferentially in p53-deficient SCCHN cells and increased the inhibitory effect of ionizing radiation on clonogenic survival in an additive manner. This evidence concerns the gene TP53 and acute promyelocytic leukemia.