Apoptosis is a physiological phenomenon occurring during embryonic development, T and B cell maturation, and endocrine-induced atrophy. It can be initiated by various agents and has been considered to be related to the expression of the oncosuppressor p53 gene. In this review, p53 gene-targeting mice were used to study the effect of p53 gene status on the induction of apoptosis in bone marrow cells by gamma-ray irradiation. The results showed that homozygous null (p53 -/-) murine bone marrow cells were more resistant to the induction of apoptosis by radiation than other genotypes (heterozygous, p53 +/- and wild type, p53 +/+). The percentage of apoptotic cells in p53 +/+ mice was about three times that in p53 -/- mice at 4 hr after 6 Gy gamma-irradiation, and the analysis of the apoptosis-characteristic DNA ladder further supported these findings. We found that the homozygous null mice also can undergo apoptosis after irradiation. This suggested that there is another independent apoptotic p53 gene mechanism in irradiated murine bone marrow cells. Thus, in murine bone marrow cells, both p53 gene-dependent and -independent apoptosis occurred after irradiation. In our previous work, an increase in survival of hemopoietic progenitor cells after irradiation in vitro in p53 gene deletion mice was observed. This increase is closely related to the inhibition of apoptosis in bone marrow cells in p53 gene deletion mice.