Therapy-induced neuroendocrine prostate cancer (t-NEPC/NEPC) arises via a reversible trans-differentiation process, referred to as ‘neuroendocrine differentiation’ (NED) [6,7], wherein PCa cells undergo a lineage switch and exhibit neuroendocrine features, characterized by the expression of neuronal markers such as enolase 2 (ENO2), chromogranin A (CHGA), and synaptophysin (SYP). The gene discussed is ENO2; the disease is posterior cortical atrophy.