Ferroptosis arises when iron-dependent phospholipid peroxidation overwhelms the system xc−–glutathione–GPX4 axis and parallel antioxidant defenses. Within tumors, however, the immune consequence of this death process depends on how iron and oxidized material move between malignant and immune compartments. Tumor-associated macrophages (TAMs) occupy this interface because they recycle iron, engulf dying cells and oxidized membranes, and modify the redox state of neighboring cells. These activities may confine injury to tumor cells, propagate lipid damage into immune cells, or protect malignant cells through vesicle cargo and antioxidant exchange. Ferroptotic death combines loss of viability with iron-dependent phospholipid peroxidation attenuated by an appropriate inhibitor, with genetic corroboration where feasible. Tumor-restricted ferroptosis can support antigen handling while macrophage and dendritic-cell functions remain intact. As oxidized material exceeds local clearance and antioxidant capacity, the same insult can impair CD8+ T cells and phagocytic macrophages and favor immune suppression. Three linked modules organize this process: iron-flux redistribution, lipid-hydroperoxide spectra and receptor sensing, and phagocytic clearance and antioxidant buffering. Iron flux identifies the first injured compartment, lipid species and receptor distribution shape the ensuing immune response, and clearance determines the duration and spread of injury. The framework thereby explains how TAM state, tumor niche, and treatment schedule redirect a common oxidative insult without proposing an additional ferroptosis execution pathway. Clinical translation will require ferroptosis to remain concentrated in the intended compartment while CD8+ T cells and homeostatic phagocytes retain function. Bulk iron, oxidative markers, and transcriptomic signatures provide complementary signals but cannot resolve the injured cell population.