This immunosuppressive microenvironment is thought to contribute significantly to the limited responsiveness to immune checkpoint inhibitor therapies in these malignancies (50, 51).These findings imply that for PCa patients with high CTSZ expression and this immunosuppressive phenotype, combination therapeutic strategies—such as simultaneously targeting tumor-associated macrophages (TAMs), Tregs, and the PD-1/PD-L1 axis—may be required to enhance immunotherapeutic efficacy. The gene discussed is CTSZ; the disease is neoplasm.