It has been almost a decade since the initial report of Olivieri et al. (Science 223, 594-597, 1984) on the phenomenon they termed "adaptive response of human lymphocytes to ionizing radiation." Although a number of reports have appeared since then, our understanding of this response is still incomplete. In this paper, the author presents an analysis of the area using published data in the literature as well as unpublished data from the author's laboratory. Most of the data come from measurements of the effects of low-dose radiation on chromatid-type aberrations induced in late S/early G2 phase cells. Exposure of lymphocytes to low doses of ionizing radiation can affect a certain fraction of aberrations induced by a subsequent high dose. Chemicals have been substituted for ionizing radiation as either inducers or challenging agents; however, their use has not provided specific information about inducing signals or target lesions. The working hypothesis in studies on adaptive response is that a repair activity is induced that acts on lesions in DNA. Although there is promising evidence that new and/or altered synthesis of proteins is required to observe reductions in aberrations, the gap between hypothesis and evidence is still wide. Co-ordinate analysis of different end points in individual cells should help to close this gap. While an adaptive response can be induced under a range of conditions, there is no good explanation for the inter/intradonor variability observed. The contributors to this variation need to be identified.