The abnormally controlled function of the erythroblastic leukemia viral oncogene homolog (ErbB), focal adhesion, hypoxia-inducible factor (HIF)-1, MAPK, p53, PI3K-Akt, and vascular endothelial growth factor (VEGF) pathways may contribute to the malignant tumorigenic and progressive processes in LC by inducing uncontrolled survival and proliferation, angiogenesis, EMT, invasion, migration, and metastasis of LC cells and tumors [118–121]. This evidence concerns the gene AKT1 and laryngotracheoesophageal cleft.