Utilizing such models will not only provide more reliable validation of PSAP/Sap C function in advanced PCa but also enable in-depth investigation into the specific molecular mechanisms by which they mediate bidirectional communication between tumor cells and key stromal partners (e.g., cancer-associated fibroblasts CAFs, tumor-associated macrophages TAMs) within the TME. The gene discussed is CCSAP; the disease is posterior cortical atrophy.