Abstract: Objective:To investigate the effect of RetroNectin on CIKs cells and the related mechanisms. Methods:Peripheral blood mononuclear cells (PBMC) were collected from patients and divided into two groups: groupⅠand group Ⅱ. Samples in group Ⅰwere seeded into culture flask precoated with RetroNec -tin and CD 3mAb to induce CIKs. While samples in groupⅡwere seeded into common culture flask. The pro-liferation of CIKs was detected by cytometric analysis. The cytotoxic activity of CIKs was determined by LDH assays. The phenotype changes and cell cycle of CIKs were identified by flow cytometry. The apoptosis of cells was detected by Annexin V/PI. Western blot was employed to detect the level of protein Vav 1. The CD49d and CD49e were blocked by anti-CD49d and anti-CD49e and the proliferation of cells was tested by cytometric analysis after the blockage. The phenotype changes of cells were identified by flow cytometry after the blockage. Results: RetroNectin enhanced the proliferation of CIKs (P<0.05). Flow cytometric analysis showed that RetroNectin significantly increased the number of CD25+ T cells (P<0.05). RN-CIK was more ac -tive than CIK in killing HCT- 8 cell lines in vitro (P<0.05). RetroNectin could block the CIKs at G 1 phase (P<0.05) and resist apoptosis. There was no significant difference in the proliferation between the two groups af -ter the blockage with CD 49d and CD 49e (P>0.05). The expression of protein Vav1 was associated with CD25+T cells. Conclusion:RetroNectin enhances the proliferation of CIKs by influencing the cell cycle, resist-ing apoptosis possibly through the site of CD 49d and CD49e, and inducing T cell activation as the second sig-naling through Vav1.