Increased radioresistance for exposures to low-LET radiation with doses exceeding a few hundred milligray is a well established fact for cell inactivation in vitro and in vivo. Cell inactivation and the subsequent replacement by intermediate cells is a possible mechanism for a radiation-induced increase of the number of intermediate cells in carcinogenesis in an irradiated organ. In the present work this mechanism has been implemented in the two-step clonal expansion model for carcinogenesis in the lung in addition to the conventionally assumed radiation-induced initiation. Compared with the original TSCE model, the new model has the same number of parameters and fits the lung cancer incidence data for the atomic bomb survivors slightly better. The resulting estimate of the lung cancer risk after low-dose exposures of persons with an age of 20 or 40 years is similar in the two models; however, it is higher by about an order of magnitude in the new model for an age-at-exposure of 60 years. Age-at-exposure dependence and risk estimates at low dose turn out to be closer to best estimates obtained with a constant-excess-relative-risk model for different age-at-exposure subgroups.