Normal development is a balance process, which includes proliferation and cell death. Indeed both proliferation and apoptotic cell death are very complex process that involves the participation of many genes. In both events, the tumor suppressor p53 is one of the most important and studied genes. This transcription factor activates several genes, which results in the arrest of the cellular cycle and cellular repair or apoptosis. Many are the signals that activate p53 function including: DNA damage by gamma or ultraviolet radiation and chemical agents and hypoxia, among others. When p53 is activated it can either induces the expression of p21 (Waf1, Cip-1), which participates in the cellular arrest between G1-S transition, or the expression of bax, PIGs, IGF-BP3, Fas, FasL and DR5. The former genes participate in the cascade of events that induce apoptosis. Cellular arrest or apoptosis depends of the degree of cellular damage. The final outcome of the different mechanisms of action of p53 is to maintain the genomic stability of the cell. Thus, the absence of this protein contributes to genomic instability, the accumulation of mutations and increased tumorigenesis. It has been demonstrated that p53 present mutations in 50-55% of all types of reported human cancer. These mutations are primary located in DNA binding domain of the protein, which results in the loss of its biological activity. Frequently, tumors that present wild type p53 have a better response towards therapy than those that present p53 mutations. This review is focused on the knowledge of the normal p53 cellular pathways and their alterations in cancer. It is clear that the understanding of p53 function in the development of this pathology may give new insights in future therapeutic strategies including gene therapy for cancer.