ZSD, administered orally, inhibited the growth of Lewis LC in a subcutaneous allograft model, increased necrosis and inflammatory cell proliferation in the tumor tissues, and caused LC cells to undergo apoptosis by downregulating the levels of p-AKT, p-GSK-3β, β-catenin, and Bcl-2. Here, AKT1 is linked to laryngotracheoesophageal cleft.