Although the underlying mechanism regarding PD-L1 regulation in OSCC remains unclear to date, the tumoural PD-L1 may be suppressed by the activation of the HIF-1A/GLUT1/EMT axis with regard to the high 18F-FDG-uptake in OSCC, this is in contrast to the PD-L1 regulation in other cancers, which are induced by the activation of the HIF-1A signal.44 Thus, these findings suggest that high 18F-FDG-uptake in OSCC may be associated with low PD-L1 expression because of the difference in PD-L1 regulation mechanisms between OSCC and other cancers. This evidence concerns the gene HIF1A and cancer.