AKT1 and esophageal squamous cell carcinoma: The present work suggested that Gli1 was activated independent of SMO via FAK/AKT pathway, where the activated AKT phosphorylated Gli1 at Ser112/Thr115/Ser116 sites, causing the dissociation of Gli1 from SuFu binding and enhancement of its activity, and resultantly inducing stemness and metastasis of ESCC.