We then mutated these potential binding motifs in the OXTR full length (pOXTR-2000) reporter construct, and the reporter assay showed that hyperglycemia-induced reporter activation disappeared in two of the ERE mutation constructs (located at −1005 and −944, respectively, marked in green, see Figure 2B), indicating that hyperglycemia mediates OXTR suppression through the ERE binding motif on the OXTR promoter (see Figure 2C). The gene discussed is OXTR; the disease is Hyperglycemia.