The identification of p53 protein as a key molecular determinant for the regulation of neuroendocrine cell proliferation and quiescence not only offers the critical link between the transformation of neuroendocrine cells and the development of prostate SCNC, but also provides a mechanistic explanation for the neuroendocrine phenotype of prostate tumors from the transgenic adenocarcinoma of mouse prostate (TRAMP) model. This evidence concerns the gene TP53 and adenocarcinoma.