For example, RB1 loss leads to an E2F1-dependent increase in the synthesis of glutathione in advanced disease, presumably protecting cancer cells from reactive oxygen species in response to therapeutic intervention, which renders these cells more reliant on glutathione metabolism for survival and sensitizes them to ferroptosis induced by glutathione-depleting agents, such as erastin and buthionine sulfoximine (55). This evidence concerns the gene E2F1 and cancer.