Ectopic adrenocorticotropin (ACTH) secretion, a rare cause of ACTH-dependent Cushing syndrome, may be caused by neuroendocrine tumors (NETS). Postoperative hypothalamic-pituitary-adrenal (HPA) axis suppression is expected due to prolonged ACTH and cortisol overproduction. Pituitary corticotrophs are suppressed, but the adrenals are hyperplastic, and cortisol is expected to rise exuberantly after ACTH stimulation. An early postoperative short Synacthen test (SST) can therefore be unreliable as a marker of the HPA axis. Recovery of corticotrophs and adrenals is unpredictable. We report a 36-year-old woman with severe Cushing syndrome. Biochemical evaluation confirmed ACTH-dependent hypercortisolism. Inferior petrosal sinus sampling was consistent with an ectopic ACTH source, and imaging revealed a 10-mm tracer-avid pulmonary lesion. Surgical excision confirmed an ACTH-secreting atypical carcinoid tumor. Postoperatively, the patient exhibited profound ACTH and cortisol deficiency and was discharged on once-daily prednisolone replacement. Seven weeks after surgery, she had an unexpectedly flat SST with undetectable cortisol levels, suggesting rapid adrenal atrophy. Gradual HPA recovery was documented with slow prednisolone withdrawal over the following year. This case demonstrates rapid adrenal atrophy and encouragingly early full HPA-axis recovery. There is no cutoff value below which adrenal recovery is impossible. A postoperative SST may hinder glucocorticoid-tapering strategies.