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. This evidence concerns the gene NR3C1 and Insulin resistance.