SOD1 and neoplasm: demonstrated that B7-H3 regulated glucose metabolism through ROS-mediated HIF1a stabilization, which contributed to B7-H3-enhanced tumor growth; B7-H3 suppresses NRF2 transcriptional activity, which in turn reduces transcription of the antioxidant enzymes SOD1, SOD2, and PRX3; B7-H3-induced ROS then stabilized HIF1α, thus increasing the expression of the glycolytic enzymes LDHA and PDK1, an effect that promoted pyruvate conversion into lactate while inhibiting pyruvate flux through the TCA cycle (71) (Figure 3), contributing to tumor metabolism microenvironment shaping (48).