These findings on the roles of RB1 in neuronal dendrite plasticity and axon regeneration and TP53 in neuron reprogramming raise questions whether similar phenotype-switching mechanisms orchestrated by RB1 or TP53 also trigger neuroendocrine phenotype switch in prostate cancer, and whether-and how-the neuron-like phenotype provides advantage for survival and protection from current anti-cancer therapies. The gene discussed is TP53; the disease is prostate cancer.