The article reviews the crosstalk between CD8+ T cells and ferroptosis in cancer. CD8+ T cells, the primary effector cells of cytotoxic T lymphocytes, play a crucial role in recognizing and killing cancer cells. Traditionally, CD8+ T cells induce cancer cell death through perforin and granzyme, as well as Fas-L/Fas binding. However, recent studies have shown that CD8+ T cell-derived IFN-γ promotes cancer cell ferroptosis by upregulating IRF1 and IRF8 and downregulating the system XC-. Ferroptosis in cancer cells enhances the anti-tumor effects of CD8+ T cells by releasing tumor-associated antigens, which activate CD8+ T cells through antigen-presenting cells (APCs). Unfortunately, intra-tumoral CD8+ T cells are more sensitive to ferroptosis than cancer cells, limiting the application of ferroptosis inducers in cancer therapy. Additionally, CD8+ T cells are susceptible to ferroptosis induced by other immune cells in the tumor microenvironment (TME), such as tumor-associated macrophages, dendritic cells, Tregs, and bone marrow-derived immunosuppressive cells. This review integrates relevant studies to reveal the potential mechanisms of crosstalk between CD8+ T cells and ferroptosis and summarizes preclinical models in cancer therapy to find new therapeutic strategies.The article reviews the crosstalk between CD8+ T cells and ferroptosis in cancer. CD8+ T cells, the primary effector cells of cytotoxic T lymphocytes, play a crucial role in recognizing and killing cancer cells. Traditionally, CD8+ T cells induce cancer cell death through perforin and granzyme, as well as Fas-L/Fas binding. However, recent studies have shown that CD8+ T cell-derived IFN-γ promotes cancer cell ferroptosis by upregulating IRF1 and IRF8 and downregulating the system XC-. Ferroptosis in cancer cells enhances the anti-tumor effects of CD8+ T cells by releasing tumor-associated antigens, which activate CD8+ T cells through antigen-presenting cells (APCs). Unfortunately, intra-tumoral CD8+ T cells are more sensitive to ferroptosis than cancer cells, limiting the application of ferroptosis inducers in cancer therapy. Additionally, CD8+ T cells are susceptible to ferroptosis induced by other immune cells in the tumor microenvironment (TME), such as tumor-associated macrophages, dendritic cells, Tregs, and bone marrow-derived immunosuppressive cells. This review integrates relevant studies to reveal the potential mechanisms of crosstalk between CD8+ T cells and ferroptosis and summarizes preclinical models in cancer therapy to find new therapeutic strategies.