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Iron- and reactive oxygen species (ROS)-dependent ferroptosis occurs in plant cells. Ca²⁺acts as a conserved key mediator to control plant immune responses. Here, we report a novel role of cytoplasmic Ca²⁺influx regulating ferroptotic cell death in rice immunity using pharmacological approaches. High Ca²⁺influx triggered iron-dependent ROS accumulation, lipid peroxidation, and subsequent hypersensitive response (HR) cell death in rice (Oryza sativa). DuringMagnaporthe oryzaeinfection, 14 different Ca²⁺influx regulators altered Ca²⁺, ROS and Fe²⁺accumulation,glutathione reductase(GR) expression, glutathione (GSH) depletion and lipid peroxidation, leading to ferroptotic cell death in rice. High Ca²⁺levels inhibited the reduction of glutathione isulphide (GSSG) to GSHin vitro. Ca²⁺chelation by ethylene glycol-bis (2-aminoethylether)-N, N, N’, N’-tetra-acetic acid (EGTA) suppressed apoplastic Ca²⁺influx in rice leaf sheaths during infection. Blocking apoplastic Ca²⁺influx into the cytoplasm by Ca²⁺chelation effectively suppressed Ca²⁺-mediated iron-dependent ROS accumulation and ferroptotic cell death. By contrast, acibenzolar-S-methyl (ASM), a plant defense activator, significantly enhanced Ca²⁺influx, as well as ROS and iron accumulation to trigger ferroptotic cell death in rice. The cytoplasmic Ca²⁺influx through calcium-permeable cation channels, including the putative resistosomes, could mediate iron- and ROS-dependent ferroptotic cell death under reducedGRexpression levels in rice immune responses.