CD8(+) T cells are considered a critical component of antitumor immunity. However, tumor-infiltrating CD8(+) T cells may express more than one checkpoint molecules that have the potential to inhibit effector responses alone or cooperatively. Here, we focused on the expression dynamic of TIGIT and PD-1 in CD8(+) T cells. TIGIT(+) subset presented significantly higher PD-1 expression than TIGIT(-) subset in circulating CD8(+) T cells. The expression dynamic of TIGIT and PD-1 was then tracked. In total CD8(+) T cells, TIGIT mRNA increased more rapidly than PD-1 mRNA, and TIGIT(+) CD8(+) T cells upregulated PD-1 more rapidly than TIGIT(-) CD8(+) T cells. Next, 24-h-stimulated CD8(+) T cells were re-sorted into TIGIT(+) and TIGIT(-) subsets, and the TIGIT(+) cells that came from TIGIT cells also presented significantly more rapid PD-1 induction than persistent TIGIT(-) CD8(+) T cells. In non-small cell lung cancer (NSCLC) patients, the expression of PD-1 was more enriched in TIGIT(+) cells than in TIGIT cells in both circulating CD8(+) T cells and tumor-infiltrating CD8(+) T cells. Function analysis revealed that TIGIT(+) CD8 T cells presented lower interferon-gamma, perforM 1, and granzyme B upregulation than TIGIT(-) CD8 T cells, especially in NSCLC patients. Overall, these data indicated that TIGIT presented earlier expression dynamic than PD-1 in activated CD8(+) T cells and was upregulated in NSCLC patients.