Abstract: The activation and regulation of nuclear factor κ B <NF-κ B> is one of such factors controlling cellular radiosensitivity are tightly controlled by Iκ B-α, a cellular inhibitory protein of NF-κ B. To assess a role of NFκ B, we constructed three different types of expression plasmids, i.e.S-Iκ B (mutations at 32, 36 Ser), Y-Iκ B (mutation at 42 Tyr) and SY-Iκ B. The cell clones expressing S-Iκ B and Y-Iκ B proteins became sensitive to Xrays as compared with the parental cells.The cell clones expressing SY-Iκ B were further radiosensitive.By the treatment with herbimycin A, an inhibitor of phosphorylation, the X-ray sensitiviity of cells expressing SY-Iκ B did not change, while that of the cells expressing S-lκ B and Y-lκ B and the parental cells was enhanced.After irradiation by X-rays, the expression of p53, which is one of factors regulated dawnstream the NF-κ B, was enhanced in parental cells, while that of those clones did not change.The inhibition of Iκ B-α phosphorylation at serine and tyrosine acts independently on the sensitization to X-rays, and the inhibition of p53 expression may play, in part, a role in the radiosensitization in these clones.