This phenomenon might be attributed to the theory that the proportion of patients with isolated PPNAD was different between our study and that by Stratakis et al. The molecular mechanism underlying the paradoxical response to dexamethasone in patients with PPNAD was due to an increased expression of glucocorticoid receptor in PPNAD nodules [17]. This evidence concerns the gene NR3C1 and primary pigmented nodular adrenocortical disease.