Immunogenic cell death (ICD) is a form of regulated cell death that enhances tumor immunogenicity and activates tumor-specific innate and adaptive immune responses. It is crucial for developing more effective cancer immunotherapies. This review discusses the mechanisms and therapeutic potential of ICD, highlighting recent findings. ICD is characterized by the release of damage-associated molecular patterns (DAMPs), which activate antigen-presenting cells (APCs) and promote immune responses. Various cell death modes, including necroptosis, ferroptosis, pyroptosis, and autosis, have been identified as ICD-like processes. For example, necroptosis involves the release of DAMPs and activation of immune cells, while ferroptosis is iron-dependent and can enhance immunogenicity. Pyroptosis, a programmed necrotic cell death, is mediated by gasdermin proteins and leads to the release of pro-inflammatory cytokines. Autosis, a form of autophagy, can also induce ICD by releasing DAMPs. Recent studies have shown that the depletion of ubiquitin-specific protease 18 (USP18) and the induction of atypical interferon (IFN)-stimulated genes (ISGs), such as polo-like kinase 2 (PLK2), can promote ICD. These findings suggest that targeting USP18 and other factors involved in ICD could be promising therapeutic strategies for cancer immunotherapy. The review also discusses the importance of ICD in both preclinical and clinical settings, emphasizing its potential to enhance anti-tumor immunity and improve therapeutic outcomes. Despite these advances, challenges remain in developing effective ICD-inducing agents and strategies for clinical application.Immunogenic cell death (ICD) is a form of regulated cell death that enhances tumor immunogenicity and activates tumor-specific innate and adaptive immune responses. It is crucial for developing more effective cancer immunotherapies. This review discusses the mechanisms and therapeutic potential of ICD, highlighting recent findings. ICD is characterized by the release of damage-associated molecular patterns (DAMPs), which activate antigen-presenting cells (APCs) and promote immune responses. Various cell death modes, including necroptosis, ferroptosis, pyroptosis, and autosis, have been identified as ICD-like processes. For example, necroptosis involves the release of DAMPs and activation of immune cells, while ferroptosis is iron-dependent and can enhance immunogenicity. Pyroptosis, a programmed necrotic cell death, is mediated by gasdermin proteins and leads to the release of pro-inflammatory cytokines. Autosis, a form of autophagy, can also induce ICD by releasing DAMPs. Recent studies have shown that the depletion of ubiquitin-specific protease 18 (USP18) and the induction of atypical interferon (IFN)-stimulated genes (ISGs), such as polo-like kinase 2 (PLK2), can promote ICD. These findings suggest that targeting USP18 and other factors involved in ICD could be promising therapeutic strategies for cancer immunotherapy. The review also discusses the importance of ICD in both preclinical and clinical settings, emphasizing its potential to enhance anti-tumor immunity and improve therapeutic outcomes. Despite these advances, challenges remain in developing effective ICD-inducing agents and strategies for clinical application.