In a mouse model of iatrogenic Cushing’s syndrome, knockout of the Dbi gene, mutation of Gabrg2, antibody-mediated neutralization of ACBP/DBI or transcriptional downregulation of ACBI/DBI by thyroid hormone all prevent the metabolic consequences of chronic glucocorticoid administration. This evidence concerns the gene GABRG2 and Cushing syndrome due to macronodular adrenal hyperplasia.