While these models have successfully uncovered the core interaction between PSAP/Sap C and AR and their capacity to activate key intracellular signaling cascades, they suffer from significant limitations: they inadequately recapitulate the complex and dynamically evolving TME found in humans, particularly failing to effectively model the intricate stromal interactions (e.g., communication with fibroblasts, immune cells), tumor heterogeneity, and adaptive responses under therapeutic pressure characteristic of the post-androgen deprivation therapy CRPC stage. The gene discussed is AR; the disease is neoplasm.