The correlation of both TP53 mutations and FOXM1 upregulation in an early stage of HNSCC development strongly indicates that the interplay of TP53 mutations and FOXM1 are pathologically relevant, in which both loss of FOXM1 repression due to p53 mutations and activation of FOXM1 expression by mutant p53 GOF play important roles contributing to HNSCC development and progression. This evidence concerns the gene TP53 and head and neck squamous cell carcinoma.