This model is based on three competing tumor subpopulations, i.e., the 3 players in the game of dominance: (i) TP, which expresses high levels of CYP17A1 enabling androgen production from serum precursors (Androgen Receptor/AR+, CYP17+ on IHC); (ii) T+, which requires exogenous androgen (AR+, CYP17− on IHC); and (iii) T−, which is androgen-independent and abiraterone-resistant (AR− and CYP17− on IHC). This evidence concerns the gene CYP17A1 and neoplasm.