HAVCR2 and neoplasm: A previous study has suggested that the loss of immunogenic neoantigens, due to mutation of the histocompatibility complex I (MHC I) molecule, and overexpression of interferon-gamma (IFN-γ)-induced T-cell-silencing ligands, such as programmed death-ligand 1 (PD-L1), lymphocyte activation gene-3 (LAG-3), and T-cell immunoglobulin and mucin domain-3 (TIM-3), after ICI treatment, can promote inhibitory signals in effector T-cells, and result in exhausted tumor-infiltrating lymphocytes (TILs) losing their ability to attack tumor cells [15,16].