This can primarily be attributed to a deregulation of EGFR itself (overexpression and strong activity in more than 80% of HNSCC) [42,43], the expression of a mutant type III variant of EGFR [44,45], aberrant downstream signaling pathways [46,47,48], an oncogenic switch [49,50,51,52] or compensatory mechanisms (such as the activity of other tyrosine-kinase receptor ALK [53], MET [54,55] or AXL [56,57]). This evidence concerns the gene AXL and head and neck squamous cell carcinoma.