For the evolution of NEPC (Figure 1), many previous studies have focused on the neuroendocrine transformation of prostate adenocarcinoma cells under the pressure of endocrine therapy, with reduced or loss of AR expression and expression of neuroendocrine markers such as synaptophysin (SYP), chromogranin A (CgA), and neuron-specific enolase (NSE), thereby transdifferentiating into NEPC (18–20). The gene discussed is ENO2; the disease is prostate adenocarcinoma.