Through cellular and molecular experiments, Chen et al. [26] found that EGFR mutations reduced the uptake of FDG in NSCLC via the NOX4/ROS/GLUT1 pathway, indicating that the uptake of 18F-FDG is related to EGFR mutation status and that it is possible to use FDG PET/CT metabolic parameters to predict tumor EGFR mutation status. The gene discussed is EGFR; the disease is neoplasm.