To rule out this possibility, we attempted to inhibit Cushing’s syndrome by two alternative methods, namely, (1) tamoxifen-inducible expression of a CRE recombinase that excises the floxed intron 2 of the gene encoding ACBP/DBI, thus leading to its conditional ablation, either at the whole-body level or in hepatocytes alone, and (2) a point mutation (F77I in subunit GABRG2) in the ACBP/DBI receptor, GABAAR, that abolishes its interaction with ACBP/DBI10,11. This evidence concerns the gene GABRG2 and Cushing syndrome due to macronodular adrenal hyperplasia.