Ferroptosis, necroptosis, and pyroptosis are three non-apoptotic cell death mechanisms that have emerged as important targets in anticancer immunity. These mechanisms, when combined with immune checkpoint inhibitors (ICIs), have shown synergistic antitumor effects, even in ICI-resistant tumors. CD8+ T cells, traditionally believed to induce tumor cell death through perforin-granzyme and Fas-FasL pathways, have also been shown to induce ferroptosis and pyroptosis, which can enhance antitumor immunity. The induction of these cell death mechanisms is associated with the release of damage-associated molecular patterns (DAMPs), which activate the immune system and promote antitumor responses. Necroptosis, ferroptosis, and pyroptosis are all involved in immunogenic cell death (ICD), a process that enhances the immune system's ability to recognize and kill tumor cells. The crosstalk between these cell death mechanisms and antitumor immunity is complex and involves multiple signaling pathways. Bioinformatic analyses have shown that the expression of genes associated with these cell death mechanisms is correlated with T cell dysfunction and CD8+ T cell infiltration. The sensitivity of tumors to these cell death mechanisms may be influenced by factors such as microsatellite instability (MSI) and tumor mutation burden (TMB). The combination of ICIs with agents that induce these cell death mechanisms may improve the efficacy of cancer treatment. However, the development of drugs that specifically activate these cell death mechanisms in humans remains a challenge. Despite this, the potential of these mechanisms in cancer therapy is promising, and further research is needed to fully understand their role in anticancer immunity.Ferroptosis, necroptosis, and pyroptosis are three non-apoptotic cell death mechanisms that have emerged as important targets in anticancer immunity. These mechanisms, when combined with immune checkpoint inhibitors (ICIs), have shown synergistic antitumor effects, even in ICI-resistant tumors. CD8+ T cells, traditionally believed to induce tumor cell death through perforin-granzyme and Fas-FasL pathways, have also been shown to induce ferroptosis and pyroptosis, which can enhance antitumor immunity. The induction of these cell death mechanisms is associated with the release of damage-associated molecular patterns (DAMPs), which activate the immune system and promote antitumor responses. Necroptosis, ferroptosis, and pyroptosis are all involved in immunogenic cell death (ICD), a process that enhances the immune system's ability to recognize and kill tumor cells. The crosstalk between these cell death mechanisms and antitumor immunity is complex and involves multiple signaling pathways. Bioinformatic analyses have shown that the expression of genes associated with these cell death mechanisms is correlated with T cell dysfunction and CD8+ T cell infiltration. The sensitivity of tumors to these cell death mechanisms may be influenced by factors such as microsatellite instability (MSI) and tumor mutation burden (TMB). The combination of ICIs with agents that induce these cell death mechanisms may improve the efficacy of cancer treatment. However, the development of drugs that specifically activate these cell death mechanisms in humans remains a challenge. Despite this, the potential of these mechanisms in cancer therapy is promising, and further research is needed to fully understand their role in anticancer immunity.