Cushing's syndrome is a challenging disease in which excess cortisol is secondary to diverse tumors with complex molecular mechanisms. The syndrome has been categorized as corticotropin-dependent or corticotropin-independent. Approximately 20% of cases — mainly cortisol-secreting unilateral adenomas or carcinomas — are considered corticotropin-independent. Cushing's syndrome rarely (in <2% of cases) results from primary bilateral nodular hyperplasia (either corticotropin-independent macronodular adrenal hyperplasia or micronodular hyperplasia). Bilateral macronodular adrenal hyperplasia with subclinical cortisol secretion is more frequent; approximately 10% of incidentally detected adrenal lesions, which are seen in approximately 4% of adults, are bilateral.1 Despite suppressed levels of circulating corticotropin, excess cortisol . . .