Simultaneously, the flow cytometric evaluation of immune cells indicated that the up-regulation of MGAT1 in cancer cells dramatically inhibited the expression of TNFα, IFNγ, and Ki-67 in CD8+ T cells, while depletion of MGAT1 dramatically enriched the expression of TNFα, IFNγ, Granzyme B, and Ki-67, indicating a potent role for MGAT1 in modulating T cell-mediated antitumor function in vitro (Fig. 2c). This evidence concerns the gene MKI67 and cancer.