The results showed that NOX activity was significantly reduced following HMGCL depletion, and NOX activity was significantly stimulated with HMGCL overexpression, suggesting that HMGCL-induced DPP4 might activate NOX1 to induce ferroptosis in HCC cells (Supplementary Fig. S8C, D). The gene discussed is NOX1; the disease is hepatocellular carcinoma.