AR and neoplasm: According to the model presented in the paper, genes like N-Myc, RB1, and TP53 aid evasion from androgen deprivation therapy in an androgen receptor-independent manner through lineage plasticity; genes like SRRM4, REST, BRN2, and FOXA1/2 play a crucial role in specific neuroendocrine differentiation of the tumor; and mediators like AURKA, PEG10, MEAF6, and Cyclin D1 allow neuroendocrine prostate cancer cells to undergo clonal expansion and develop treatment resistance.