This review discusses the mechanisms of metabolic cell death, including ferroptosis, cuproptosis, disulfidptosis, lysozincrosis, and alkaliptosis, and explores their potential in cancer therapy. Ferroptosis, a form of iron-dependent cell death, is characterized by the accumulation of lipid peroxides on cellular membranes. The review delves into lipid synthesis and peroxidation, iron metabolism, and defense mechanisms against ferroptosis, such as GPX4-dependent and GPX4-independent pathways. Cuproptosis, triggered by excessive cellular copper levels, involves the toxic gain-of-function effect of protein lipoylation. The review also examines the role of copper ionophores in inducing cuproptosis and their potential in cancer therapy. Disulfidptosis, a form of cell death resulting from excessive disulfide stress, is another regulated cell death modality discussed. The review highlights the complexity of these metabolic cell death pathways and their potential as innovative therapeutic avenues for cancer treatment.This review discusses the mechanisms of metabolic cell death, including ferroptosis, cuproptosis, disulfidptosis, lysozincrosis, and alkaliptosis, and explores their potential in cancer therapy. Ferroptosis, a form of iron-dependent cell death, is characterized by the accumulation of lipid peroxides on cellular membranes. The review delves into lipid synthesis and peroxidation, iron metabolism, and defense mechanisms against ferroptosis, such as GPX4-dependent and GPX4-independent pathways. Cuproptosis, triggered by excessive cellular copper levels, involves the toxic gain-of-function effect of protein lipoylation. The review also examines the role of copper ionophores in inducing cuproptosis and their potential in cancer therapy. Disulfidptosis, a form of cell death resulting from excessive disulfide stress, is another regulated cell death modality discussed. The review highlights the complexity of these metabolic cell death pathways and their potential as innovative therapeutic avenues for cancer treatment.