The body itself can secrete glucocorticoids, also known as adrenocorticotropic hormones, because they are secreted by the adrenal cortex and regulate glucose metabolism. Glucocorticoids have a very powerful anti-inflammatory effect in larger doses, protecting the body from inflammatory reactions, as well as suppressing immune responses and combating shock, and are therefore used to treat a variety of inflammatory conditions, autoimmune diseases and other disorders. Although these drugs are very effective, they can have many side effects, such as abnormal accumulation of adipose tissue, the mechanisms of which are still not clearly understood. Recently, researchers from NIH found that glucocorticoids can directly regulate the transcription factor Foxa3 in adipose tissue and induce excessive accumulation of adipose tissue through Foxa3. The results of the study were published in the international academic journal PNAS. Previous studies have found that the transcription factor Foxa3 has a role in promoting the enlargement of visceral adipose tissue and suppressing energy expenditure, and that the expression level of Foxa3 in adipose tissue is gradually increased by high-fat diet and age, but no studies have been conducted to elaborate the regulatory mechanism of Foxa3 in adipose tissue. In this study, researchers used computational prediction analysis combined with molecular studies to find that Foxa3 in precursor adipocytes, mature adipocytes and adipose tissue is regulated by the glucocorticoid receptor, and that Foxa3 also promotes the binding of the glucocorticoid receptor to target gene promoters in adipose tissue. Using mice, the researchers analyzed the long-term effects of drug treatment with dexamethasone, a glucocorticoid, and showed that in the absence of Foxa3, mice specifically resisted fat accumulation, but did not improve pathological side effects in the liver, muscle, and spleen. This study demonstrates for the first time that Foxa3 in adipose tissue is a direct target of glucocorticoids and that Foxa3 plays an important role in glucocorticoid-induced adipose tissue accumulation, which has important implications for the improvement of glucocorticoid side effects and the development of new glucocorticoid drugs that avoid the development of adipose accumulation.