Meanwhile, the selection pressure and lineage plasticity of AR‐pathway inhibition can lead to neuroendocrine differentiation of CRPC, as is the case with bulky metastatic disease that has low serum PSA levels.31 Elevated neuron‐specific enolase (NSE) and circulating chromogranin A (CgA) have been reported as possible biological markers in which the role of PSMA imaging remains unclear. Here, FOLH1 is linked to metastatic neoplasm.