Taken together, these diverse outcomes reflect the heterogeneity of tumor biology—variations in the immune microenvironment, angiogenic dependencies, and adaptive resistance mechanisms such as upregulation of alternative checkpoints (e.g., TIM-3, LAG-3), metabolic reprogramming (e.g., adenosine, IDO pathways), and engagement of redundant pro-angiogenic axes (FGF, MET, AXL). This evidence concerns the gene HAVCR2 and neoplasm.