Tumor clonal populations vary in expressing key regulators of ferroptosis, cuproptosis, disulfidptosis, lysozincrosis, and alkaliptosis, leading to unequal sensitivity to these death triggers—for instance, HNC subclones with high GPX4 are intrinsically resistant to ferroptosis [64], while variability in FDX1 or TRPML1 affects susceptibility. This evidence concerns the gene GPX4 and neoplasm.