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The goal of these studies was to investigate the potential for low dose ionizing radiation to modify Bax induced oncogenesis. Bax is a regulator of apoptotsis as well as a regulator of prooxident function and outer mitochondrial membrane permeability. Transgenic mice which over express one or two copies of Lck-Bax gene were treated with low doses (0, 10 and 100 cGy) of low LET radiation. The insertion and overexpression of the Bax gene appears to dominate the effect upon the phenotype in that the higher the gene dose the faster and more likely is the onset of thymic lymphoma. Mice grouped by radiation dosage potentially offer some insight. The double transgenic mice appear to be unaffected by the exposure to the radiation used in this study. While not statistically significant, there appears to be a trend in the single transgenic mice that the exposure to radiation at either level (10 or 100 cGy) will shorten the life span of the mice. Paradoxically, the shortest survival times in the Lck-Bax 1 mice appear with the lowest radiation dose implying some adaptive response. Further investigation demonstrated this effect is gender specific in the Lck-Bax 1 mice. A pairwise comparison between the 0.1 Gy and 0 Gy irradiated female Lck-Bax 1 mice show a statistically significant acceleration of lymphoma formation. This difference is not seen in any of the other pairwise comparisons of female mice. Furthermore , this trend is not present in the Lck-Bax 1 male mice.