Next, we used AMG487 (anti-CXCR3 drug) to blockade the CXCR3 in vivo, and observed that the efficacy of CIK treatment was significantly inhibited (0% of tumors in CIK + AMG487 group was effectively controlled), exhausted T cells were significantly increased, and the number of tumor-infiltrating CD8+ and CD8+CD56+ T cells were also significantly reduced (Fig. 2G–K and Supplementary Fig. S3). Here, NCAM1 is linked to neoplasm.