Not only did we observe a higher degree of phenotypic heterogeneity in castrate–resistant PRAD and NEPC than previously anticipated, but also found that the expression of molecules targeted therapeutically, namely PSMA, STEAP1, STEAP2, TROP2, CEACAM5, and DLL3, varied within a subset of gene–regulatory networks (GRNs). The gene discussed is STEAP1; the disease is prostate adenocarcinoma.