However, whether the inhibition of GR by TAZ plays a role in the regulation of hepatic gluconeogenesis in some or all of these abnormal states, and whether a non-tumorigenic TAZ mutant(s), or small peptide(s) or molecule(s), which would mimic or enhance the TAZ-GR interaction could normalize the hyperglycemia associated with obesity, insulin resistance, or the chronic use of GCs, should be determined in future investigations. The gene discussed is NR3C1; the disease is obesity due to melanocortin 4 receptor deficiency.