In addition to genetic and epigenetic manipulation, the occurrence and development of CRC are significantly influenced by the tumor microenvironment (TME), which comprises immune checkpoints such as programmed death1 (PD-1) / programmed death-ligand 1 (PD-L1), LAG-3, CTLA4, and TIM3 that infiltrate immunosuppressive myeloid cells and regulatory T cells, thereby suppressing endogenous anti-tumor immunity and the effects of CAR-T therapy [10]. Here, HAVCR2 is linked to neoplasm.