CD8+ T cells and ferroptosis play critical roles in cancer immunotherapy. CD8+ T cells are key effector cells that recognize and kill cancer cells, traditionally through perforin, granzyme, and Fas-L/Fas pathways. Recent studies show that CD8+ T cell-derived IFN-γ promotes cancer cell ferroptosis via multiple mechanisms, including upregulation of IRF1 and IRF8, and downregulation of system XC-. Ferroptosis, an iron-dependent form of programmed cell death, is characterized by lipid peroxidation and glutathione depletion. Cancer cell ferroptosis can enhance CD8+ T cell anti-tumor effects by heating the tumor microenvironment through the release of tumor-associated antigens, creating a positive feedback loop. However, CD8+ T cells are more sensitive to ferroptosis than cancer cells, limiting the application of ferroptosis inducers. Additionally, CD8+ T cells can be regulated by other immune cells, such as tumor-associated macrophages, dendritic cells, Tregs, and bone marrow-derived immunosuppressive cells, which can influence their function. The interaction between CD8+ T cells and ferroptosis in cancer forms a complex network that affects tumor suppression. CD8+ T cell-derived IFN-γ promotes cancer cell ferroptosis, which in turn activates CD8+ T cells through antigen-presenting cells, enhancing anti-cancer immunity. Ferroptosis of CD8+ T cells can lead to immune evasion, while ferroptosis of cancer cells can enhance CD8+ T cell activity. The sensitivity of CD8+ T cells to ferroptosis is influenced by factors such as the TME metabolic state and the expression of ferroptosis-related genes. CD8+ T cells can also evade ferroptosis by adjusting their gene expression. The interaction between CD8+ T cells and cancer cell ferroptosis is mutually beneficial, with IFN-γ inducing cancer cell ferroptosis and cancer cell ferroptosis activating CD8+ T cells. Ferroptosis of cancer cells releases DAMPs, which activate APCs and CD8+ T cells, enhancing tumor suppression. However, ferroptosis of CD8+ T cells can impair their function. The application of ferroptosis in cancer therapy is promising, with strategies such as targeting cancer cell ferroptosis and using nanotechnology to deliver drugs that induce ferroptosis and enhance immune responses. Targeting both CD8+ T cells and cancer cell ferroptosis can amplify tumor suppression. The complex interplay between CD8+ T cells and ferroptosis in cancer highlights the need for further research to optimize therapeutic strategies.CD8+ T cells and ferroptosis play critical roles in cancer immunotherapy. CD8+ T cells are key effector cells that recognize and kill cancer cells, traditionally through perforin, granzyme, and Fas-L/Fas pathways. Recent studies show that CD8+ T cell-derived IFN-γ promotes cancer cell ferroptosis via multiple mechanisms, including upregulation of IRF1 and IRF8, and downregulation of system XC-. Ferroptosis, an iron-dependent form of programmed cell death, is characterized by lipid peroxidation and glutathione depletion. Cancer cell ferroptosis can enhance CD8+ T cell anti-tumor effects by heating the tumor microenvironment through the release of tumor-associated antigens, creating a positive feedback loop. However, CD8+ T cells are more sensitive to ferroptosis than cancer cells, limiting the application of ferroptosis inducers. Additionally, CD8+ T cells can be regulated by other immune cells, such as tumor-associated macrophages, dendritic cells, Tregs, and bone marrow-derived immunosuppressive cells, which can influence their function. The interaction between CD8+ T cells and ferroptosis in cancer forms a complex network that affects tumor suppression. CD8+ T cell-derived IFN-γ promotes cancer cell ferroptosis, which in turn activates CD8+ T cells through antigen-presenting cells, enhancing anti-cancer immunity. Ferroptosis of CD8+ T cells can lead to immune evasion, while ferroptosis of cancer cells can enhance CD8+ T cell activity. The sensitivity of CD8+ T cells to ferroptosis is influenced by factors such as the TME metabolic state and the expression of ferroptosis-related genes. CD8+ T cells can also evade ferroptosis by adjusting their gene expression. The interaction between CD8+ T cells and cancer cell ferroptosis is mutually beneficial, with IFN-γ inducing cancer cell ferroptosis and cancer cell ferroptosis activating CD8+ T cells. Ferroptosis of cancer cells releases DAMPs, which activate APCs and CD8+ T cells, enhancing tumor suppression. However, ferroptosis of CD8+ T cells can impair their function. The application of ferroptosis in cancer therapy is promising, with strategies such as targeting cancer cell ferroptosis and using nanotechnology to deliver drugs that induce ferroptosis and enhance immune responses. Targeting both CD8+ T cells and cancer cell ferroptosis can amplify tumor suppression. The complex interplay between CD8+ T cells and ferroptosis in cancer highlights the need for further research to optimize therapeutic strategies.