Currently attention has focused on understanding the mechanism(s) of action of ligand:receptor pairs which regulate immune reactivity at key “checkpoints.” Within the tumor environment overexpression of molecules expressed by T cells including cytotoxic T‐lymphocyte antigen 4 (CTLA‐4), programmed death‐1 (PD‐1), lymphocyte activation gene‐3 (LAG‐3), and T‐cell immunoglobulin and mucin‐containing protein 3 (Tim‐3) have been linked to hyporesponsiveness in T‐cell activity (T‐cell exhaustion). This evidence concerns the gene HAVCR2 and neoplasm.