Given that the P53/Rb1 model progresses toward an undifferentiated neuroendocrine phenotype with lower SLIT expression, these results support the idea that SLIT/ROBO signaling may have subtype-specific roles in prostate cancer and could be more relevant in adenocarcinomas with preserved stromal architecture compared to neuroendocrine tumors. The gene discussed is TP53; the disease is prostate carcinoma.