The molecular mechanisms underlying loss of normal expression of E-cad in human gastric cancer include promoter hypermethylation [55], somatic and germline mutations [56,57], activation of E-cad transcriptional repressors (e.g., Snail and Slug) [58,59], and reduced or lost expression of a few microRNAs (e.g., miR-200 family and miR-101) [60,61]. The gene discussed is SNAI1; the disease is gastric cancer.