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Malignant progression and limited therapeutic response in gastric cancer (GC) cannot be explained solely by increased proliferation or oncogenic alterations. Instead, they reflect how tumor cells regulate their death threshold under sustained damage, metabolic stress and immune pressure. Evidence indicates that GC cells largely retain the capacity for cell death but reduce its effective execution by attenuating signal propagation, weakening key execution steps and altering microenvironmental interactions. As a result, cellular stress persists without effective clearance, promoting survival, resistance and metastasis. The present review synthesized current evidence on the mechanisms and interplay of cell death in GC, with emphasis on their relationships with the tumor microenvironment, host factors and therapeutic stress. It further evaluated their implications for resistance, patient stratification and therapeutic intervention. Reframing GC through the lens of cell death regulation provides a more coherent basis for understanding its biological heterogeneity and for improving therapeutic strategies.