Here, we showed that multi-specific ERBB2-CAR CIK cell therapy could eliminate low tumor load and that ERBB2-CAR CIK cells could be used as a vehicle for delivering preferentially TH-1 cytokines and chemokines directly to tumor sites, which are involved in regulating innate and adaptive immunities and may have allowed T, NK, and T-NK cells to proliferate, persist, and survive in vivo, which is in contrast to IL-15 activated WT CIK cells and conventional IL-2-activated CIK cells reported by others (53). This evidence concerns the gene ERBB2 and neoplasm.