Once RSL3@COF-Fc is endocytosed by tumor cells, the progressively released methyl (1S,3R)-2-(2-chloroacetyl)-1-(4-(methoxycarbonyl)phenyl)-2,3,4,9-tetrahydro-1H-pyrido[3,4-b]indole-3-carboxylate (RSL3) inhibits GPX4 (a central checkpoint of the antioxidant system of the tumor cells) to perturb the redox homeostasis, whereas the Fc induces the production of •OH via Fenton-like reactions, leading to lipid peroxidation (Figure 2C) 93. This evidence concerns the gene GPX4 and neoplasm.