In fact, since HG promotes the upregulation of mesenchymal markers (i.e., FSP-1, SM22, and α-SMA) and the downregulation of H19 and endothelial cell markers (i.e., CD-31 and VE-CAD), the overexpression of H19 in HG-treated HRECs dramatically reversed the trends evoked by hyperglycemia, which is suggestive of a protective role for H19 in preventing EndMT in DR. This evidence concerns the gene H19 and Hyperglycemia.