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After EZH2 inhibitor treatment, tumor cells undergo significant lipid metabolic reprogramming [164], activating the SLC7A11/GPX4 antioxidant axis and upregulating lipid/cholesterol synthesis-related genes (e.g., Stearoyl-CoA Desaturase 1, SCD1), thereby resisting ferroptosis and limiting the efficacy of EZH2 inhibitors