When cultured human lymphocytes were treated with a radiomimetic chemical bleomycin, metaphase chromosomes from different individuals exhibited a wide spectrum of responses in terms of number of chromatid lesions. This variability is interpreted as the result of capability for DNA repair. Among 100 healthy, normal individuals tested, nearly 60% showed a mean breaks per cell rate in the range of 0.20-0.60, whereas, only 12% showed breaks per cell rates above 1.00. On the other hand, among 75 cancer patients, 60% showed breaks per cell rates above 1.00. It is believed that differential responses to a mutagen have genetic implications. Individuals with DNA repair deficiencies may be more susceptible to carcinogens and, therefore, are more susceptible to neoplastic induction.