Together with our previous observation that GOF mutant p53s inhibit AMPK [16], our current study strongly suggests that GOF mutant p53s can activate FOXM1 through inhibiting AMPK and its downstream target FOXO3a (Fig. 7k) and that the mutant p53-AMPK-FOXO3a-FOXM1 signaling axis is one of mechanisms through which mutant p53s gain oncogenic activity in HNSCC. This evidence concerns the gene FOXM1 and head and neck squamous cell carcinoma.