Other studies have also described nonclassical mechanisms of IGF1R signaling, demonstrating that IGF1 ligand binding directly to αvβ3 and α6β4 integrins is necessary for downstream signaling (36, 37) and that FAK, a major signaling kinase localized to matrix adhesions, is activated by IGF1 in HNSCC cells, leading to cell growth and suppressed apoptosis (38, 39). This evidence concerns the gene IGF1 and head and neck squamous cell carcinoma.