These findings uncover a dual cooperative mechanism by which PLS3 remodels the immune microenvironment: on the one hand, it downregulates immune checkpoint molecules to alleviate immunosuppression; on the other hand, it disrupts chemokine-receptor axes (e.g., CCL19-CCR7), thereby blocking effector immune cell recruitment and synergistically establishing an immune-privileged niche that fuels tumor progression. The gene discussed is CCR7; the disease is neoplasm.