Our studies of QKI-5-overexpression, QKI-5-knockdown and β-catenin synthesis inhibition revealed that QKI-5 did not change the levels of DKK3, DVL1, DVL3 and GSK3β as Wnt/β-catenin signaling regulators in LC cells, but could accelerate the phosphorylation and ubiquitin-dependent degradation of β-catenin through increasing p-GSK3β, therefore decreasing β-catenin in LC cells. The gene discussed is DVL1; the disease is laryngotracheoesophageal cleft.