In summary, this study found that H19 promoted EMT formation in CRC through H19/miR-138/Vimentin and H19/miR-200a/ZEB1/2 ceRNA networks [58], by which: 1) H19 acted as a ceRNA to compete for free miR-138 and miR-200a, which sequestered these two miRNA species and freed the 3′UTR of targeted mRNAs; 2) due to the competitive binding events, H19 abolished the suppressive effect on Vimentin and ZEB1/2. This evidence concerns the gene VIM and colorectal carcinoma.