In cell populations was produced by the superposition of cell-to-cell variability in the dynamics of p53. Damped oscillation normally indicates that a biological system is in a relaxed stable state, which is the genesis of the maintenance of homeostasis. In our simulated results, the stochasticity of intranuclear biochemical reaction processes induced heterogeneity and homogeneity of p53 dynamics in single cells and cell populations, respectively. This finding implies that the stochasticity of intranuclear biochemical reaction processes contributes to the implicit spontaneous ordering observed in biological multilayered systems of higher organisms. From the perspective of systems biology, it was reported that stochasticity or fluctuation of biochemical reaction processes enhanced the stability of biological functions. This finding is in good agreement with our findings based on our simulated results. Thus, consideration of the stochasticity of intranuclear biochemical reaction processes was indispensable for enabling the proposed model to realize the variability of p53 dynamics at both the single-cell and cell population levels. The proposed model, which implements such an implicit interlayer regulatory mechanism between cells and tissues, is useful for enhancing the understanding of the dynamic behavior of the cell fate decision mechanism in comparison with other conventional models. Although the simulated results by conventional models showed a tendency of decline in SF with increasing IR-dose, there was no comparison of the simulated results with experimentally observed data. In contrast, our simulated results were consistent to observed data in human fibrosarcoma cell line, which implied that the proposed model was more quantitative than conventional models. The hybrid simulation based on the proposed model has the potential to realize the variability in intrinsic apoptosis induction. Next, we explored the relationship between the number of p53 pulses and apoptosis induction. In addition, the numerical instability of the part of ordinary differential equations in the proposed model was not detected among 1000 simulations. It suggested that the proposed model was robust within the scope of mathematical analysis in this study. Cellular responses to stressors normally depend on stress intensity and are regulated by the p53 signaling network. Low-intensity stress activates p53 that induces the synthesis of p21; p21 then inhibits cyclin/cyclin-dependent kinase complexes, the cell cycle engines, leading to cell cycle arrest. During this arrest, p53 also activates the DNA repair system. In contrast, highintensity stress activates p53 that induces apoptosis in addition to cell cycle BYL719 arrest and DNA repair. p53 induces the intrinsic mitochondria-dependent apoptotic pathway. These biological findings are in qualitative agreement with our simulated results, which showed that a higher IR dose increased the number of p53 pulses as well as the potential for intrinsic mitochondriadependent apoptosis induction. Since the p53pp is final reactant in the p53 signaling network, individual variability in p53 signaling network quantitatively has an impact.