These biological findings imply that apoptosis induction at the single-cell level depends on the stochastic behaviors of intranuclear biological reaction processes generated in the p53 signaling network, including DSB generation and repair. In silico experiments using mathematical modeling and mathematical analysis are one available method of understanding the cell fate decision mechanism as a result of fluctuations of those cellular responses, i.e., cell-to-cell variability in p53 pulses and apoptosis induction under conditions of various stress intensities. Several mathematical models have been used to explore the mechanism by which the dynamics of p53 affect cell cycle arrest and apoptosis induction. Till date, one prominent finding was reported by Zhang et al.; they constructed an integrative model of four modules—generation and repair of IR-induced DSBs module, ATM switch module, p53-Mdm2 oscillator module, and cell fate decision module—and reported the possibility that stochasticity in DSB generation led to cell-to-cell variability in cell fate. However, Zhang’s model did not take into consideration any stochasticity in the generation of the p53 pulse, and the question of whether any effect of IR dose is observed on the dynamics of the p53 signaling network remained unanswered. The cell fate decision mechanism consists of several signal transduction systems that extend into two spaces, the nucleus and cytoplasm. In general, the Tubulin Acetylation Inducer existing probability of intranuclear proteins is much smaller than that of cytoplasmic proteins. Hence, the intranuclear biochemical reaction processes develop notable fluctuations compared with the cytoplasmic ones. We inferred that stochasticity in the dynamics of the p53 signaling network also has a profound relationship with cell-to-cell variability in cell fate. This hypothesis is in agreement with the implication based on the abovementioned biological findings. It is well known that stochastic simulation is useful for exploring the emergence and collapse of biological functions. Our novel mathematical model, which realized stochasticity in both the generation and repair of DSB and the p53 signaling network, has the potential to elucidate the dynamic behavior of the cell fate decision mechanism under conditions of various stress intensities. In this paper, we describe the construction of a massive integrative model that consists of the generation of IR-induced DSB, DSB repair system, p53 signaling network, and apoptosis induction pathway. These, except for the apoptosis induction pathway, are described as intranuclear biochemical reactions. Because they are modeled as stochastic processes, intrinsic noise is introduced into the simulation of intranuclear reactions. In contrast, the apoptosis induction pathway is described as cytoplasmic reactions and is modeled as a deterministic process.