This review explores the crosstalk between distinct cell death mechanisms—necroptosis, ferroptosis, and pyroptosis—and anticancer immunity. Recent studies have shown that these non-apoptotic cell death modalities can enhance the efficacy of immune checkpoint inhibitors (ICIs) in cancer treatment, even in ICI-resistant tumors. The induction of pyroptosis, ferroptosis, and necroptosis in tumor cells has been found to synergistically improve antitumor activity. CD8+ T cells, traditionally believed to induce tumor cell death through perforin-granzyme and Fas-FasL pathways, have also been shown to suppress tumor growth by inducing ferroptosis and pyroptosis. The review highlights the potential of combining these cell death mechanisms with ICIs to overcome resistance and improve patient outcomes. Additionally, the authors discuss the clinical translation of these findings, including the use of approved drugs that induce these cell death mechanisms and their potential combinations with ICIs. Bioinformatic evidence from human tissues supports the role of necroptosis, ferroptosis, and pyroptosis in enhancing CD8+ T cell infiltration and improving the efficacy of ICIs. The review concludes by emphasizing the need for clinical trials to test these promising strategies in patients.This review explores the crosstalk between distinct cell death mechanisms—necroptosis, ferroptosis, and pyroptosis—and anticancer immunity. Recent studies have shown that these non-apoptotic cell death modalities can enhance the efficacy of immune checkpoint inhibitors (ICIs) in cancer treatment, even in ICI-resistant tumors. The induction of pyroptosis, ferroptosis, and necroptosis in tumor cells has been found to synergistically improve antitumor activity. CD8+ T cells, traditionally believed to induce tumor cell death through perforin-granzyme and Fas-FasL pathways, have also been shown to suppress tumor growth by inducing ferroptosis and pyroptosis. The review highlights the potential of combining these cell death mechanisms with ICIs to overcome resistance and improve patient outcomes. Additionally, the authors discuss the clinical translation of these findings, including the use of approved drugs that induce these cell death mechanisms and their potential combinations with ICIs. Bioinformatic evidence from human tissues supports the role of necroptosis, ferroptosis, and pyroptosis in enhancing CD8+ T cell infiltration and improving the efficacy of ICIs. The review concludes by emphasizing the need for clinical trials to test these promising strategies in patients.