As CD56-positive T cells were more activated and exerted a more potent anti-tumor effect, Zou et al. discovered a novel iCAR simultaneously targeting inhibitory receptors PD-1, Tim-3, and Lag-3, which are known to be overexpressed in tumor-infiltrating lymphocytes (TILs), resulting in the upregulation of CD56 and enhancing the infiltration and anti-tumor function of CAR-T cells [97,98]. Here, HAVCR2 is linked to neoplasm.