Extensive evidence has highlighted that dysfunctional tumor-killing T cells with high expression of immune inhibitory molecules, including PD-1, CTLA4, T cell membrane protein-3 (TIM-3), T cell immunoreceptor with immunoglobulin and ITIM domains (TIGIT), and lymphocyte-activation gene-3 (LAG-3), play crucial roles in non-response to ICB therapy within the TME (5). This evidence concerns the gene HAVCR2 and neoplasm.