The clinical significance of the Wnt/β-catenin pathway in promoting the CSC phenotype is supported by the analysis of human lung cancer samples, which shows that high-grade primary and metastatic cancers have higher levels of CD133 and nuclear fractions of β-catenin and Twist1, while E-cadherin and Sox15 levels are significantly decreased compared to low-grade primary cancers [120]. The gene discussed is CDH1; the disease is lung cancer.