The peripheral lymphocytes from 7 patients affected with ataxia telangiectasia (AT) were found to be about twice as sensitive to the induction of chromatid-type aberrations by X-rays administered during the G2 phase of the cell cycle as cells from normal controls. Peripheral lymphocytes from 6 AT heterozygotes were no more sensitive than the controls. Using labelling of peripheral lymphocytes with tritiated thymidine, followed by autoradiography, it was determined that cells from affected patients, heterozygotes and normal controls, whether irradiated or not, all had similar percent labeled mitoses (PLM) curves, so the increased induced aberration yields seen in the AT cells is not simply the consequence of a longer than normal G2 phase, nor of G2 delay induced by the radiation. Peripheral lymphocytes from two affected patients and two controls were irradiated in culture, labeled with tritiated thymidine and collected with colcemid over various intervals so that by scoring unlabeled cells in autoradiographs the time course of aberration yield over all of G2 could be determined. The curve for chromatid aberrations for the AT cells differ significantly from that for the controls in intercept, suggesting that in the AT cells the radiation induces more lesions capable of resulting in aberrations, but that their repair may be similar.