A more pronounced phenotype has been reported in patients with PBMAH and germline ARMC5 pathogenic variant than in wild-type patients [13, 20, 48], with regard to the intensity of Cushing’s syndrome according to the usual endocrine and clinical markers of cortisol excess: elevated 24-h urinary free cortisol, morning plasma cortisol after 1 mg DST, and midnight plasma cortisol, associated with a more suppressed ACTH. The gene discussed is ARMC5; the disease is Cushing syndrome.