Thus, it would appear that CTNND-genes play key tumor suppressor roles in both types of esophageal cancer, with their inactivation being mediated by potentially different molecular mechanisms (promoter hypermethylation in the case of CTNND2 and deletion in the case of CTNND1), which is possibly related to the different etiology of EAC vs ESCC. This evidence concerns the gene CTNND1 and neoplasm.