This prevents the accumulation of lipid peroxides, thereby averting membrane rupture and the subsequent onset of cellular ferroptosis.[27] Although the SLC7A11-GSH-GPX4 axis is thought to be a critical mechanism for intracellular ferroptosis defense, certain cancer cell lines remain resistant to ferroptosis even after GPX4 inactivation,[52] indicating the existence of alternative defense mechanisms that are GPX4-independent.[48]. The gene discussed is GPX4; the disease is cancer.