Metabolic reprograming has an essential role in the regulation of CD8+ T cell function and its differentiation. In particular, glucose metabolism is one of the resources to hallmarks of effector T cell. It’s currently reported a new role for the glycolytic metabolite phosphoenolpyruvate (PEP) in sustaining T cell receptor-mediated Ca2+-NFAT signaling and effector functions by repressing sarco/ER Ca2+-ATPase (SERCA) activity. Based on these metabolic perspectives, we characterized peripheral CD8+ T cells of patients in different Stage of gastric cancer with both a cytokine productivity and intracellular Ca2+ levels on the stimulation of PMA/inomycin. Moreover, we assessed the basal metabolism of CD8+ T cells in each patient by Seahorse Flux Analyzer. We observed the reduction of cytokine productivity and lower levels of Ca2+ in CD8+ T cells as the progression of cancer. Flux analyzer analysis revealed a much lower glycolytic activity (extracellular acidification rate, ECAR) of CD8+ T cells in patients with Stage III or IV. These results suggested that cancer progression associates with metabolic dysregulation of peripheral CD8+ T cells function in gastric cancer patients.