For example, the GLI pathogenesis-related 2 has a fold change of -1.8 in our dataset; curiously, it has been reported that GLIPR-2 is elevated in the kidneys of patients affected by DN [89] and that miR-30e targeting GLIPR-2 is downregulated in DN, while its overexpression inhibits GLIPR-2, thus protecting from renal fibrosis in DN [90]. This evidence concerns the gene GLI1 and renal fibrosis.