CCR4-NOT transcription complex, subunit 7(CNOT7) serving as the predominant deadenylase in all eukaryotes, has great function in regulating transcription and mRNA degradation, and it has been shown to correlate with poor prognosis in the tissues of Hepatocellular carcinoma. Silencing the CNOT7 gene can up-regulate the expression of the subset of STAT1 regulatory genes with its downstream chemokine IP-10 through enhancing the occupation of the basic promoter of STAT1 .In peripheral blood circulation, the immune cells γδT could be induced to migrate to the specific areas through the chemokine receptor CXCR3 which presents in γδT , bind with the chemokine IP-10.Based on this basic , we hypothesize that silencing the CNOT7 gene in HCC cells could induce the directional homing of immune cells γδT to cancer tissues to exert an anti-tumor effect through up-regulating the expression of local STAT1 and IP-10. To verify the hypothesis, we designed an experiment about the CNOT7 gene silenced in HepG2 cell line in vitro, and then we analyzed the expression of STAT1, IP-10, and the expression of CXCR3 in γδT cells after being amplified. Besides, we also analyzed the effect of the expression product of STAT1, pSTAT1, IP-10 and CXCR3 on γδT chemotactic ability. In conclusion, our results suggest that the expression of IP-10 and chemotaxis of γδT cells could be up-regulated by silencing CNOT7 of HepG2 cells in vitro.