Furthermore, we found that CTL-persisters upregulate NRF2 and its target SLC7A11, a component of the anti-ferroptosis cystine/glutamate antiporter system xc-, while drug-persisters downregulate SLC7A11, reflecting a ferroptosis-protective state in CTL-persisters (Figures 4G and S2F).67 This finding suggests that induction of ferroptosis may be ineffective in killing residual tumor cells which survive immunotherapy. The gene discussed is SLC7A11; the disease is neoplasm.