A 70-year-old Thai man was diagnosed with stage IVB NSCLC with pleural and liver metastases. The patient’s medical history was unremarkable until December 2018, when he had right pruritic chest pain and nonproductive cough. The patient had smoked cigarettes (20 packs per year) and did not have a drinking habit. The patient had good performance status, and he was not taking any medications. He was found to have high levels of PD-L1 expression (tumor proportion score ≥ 50%) but had a negative result for epidermal growth factor receptor mutations and anaplastic lymphoma kinase rearrangement. He was treated with a combination of pembrolizumab 200 mg every 3 weeks and ipilimumab 1 mg/kg every 6 weeks. A combination of PD-1 and CTLA-4 inhibitors was used as a first-line treatment in this patient because the available evidence suggested that combination therapy may produce a higher tumor response rate than PD-1 inhibitors alone in metastatic NSCLC PD-L1 positive subgroups []. After 14 weeks of treatment, the fifth cycle of pembrolizumab and the third cycle of ipilimumab, he presented with complaints of fatigue, vigorous nausea, and vomiting without abdominal pain. His physical examination revealed his body temperature was 37.2 °C, blood pressure was 100/60 mmHg, pulse rate was 116 beats per minute, and respiratory rates was 20 breaths per minute. The examination of his abdomen, neurological system, and other systems was unremarkable. The patient’s random plasma glucose level was 794 mg/dl, and his serum ketone level was 6.3 mmol/L. His arterial blood gas analysis showed a pH of 7.17. He was admitted to the hospital, and the results of further laboratory investigations are shown in Table. Hyperglycemia, high serum ketone, low bicarbonate at 13 mmol/L, and high anion gap at 24 mmol/L were compatible with the DKA criteria. A treatment protocol for DKA with aggressive intravenous hydration and continuous intravenous insulin was initiated with a favorable outcome within 10 hours. The diagnosis of ICI-related DM was suspected due to the abrupt onset of DM. Blood analysis revealed an undetectable C-peptide level and a negative result of glutamic acid decarboxylase autoantibodies (anti-GAD) and anti–tyrosine phosphatase-like islet antigen 2. Despite his hyperglycemia improving, he still had persistent nausea and hyponatremia (serum sodium 126 mmol/L). Further investigations revealed a very low morning cortisol level (0.8 μg/dl) and normal adrenocorticotropic hormone (ACTH) level (21.7 pg/ml; normal range 0–46). His other pituitary hormone levels were normal, except for mild elevation of follicle-stimulating hormone/luteinizing hormone. He was diagnosed with IAD and immediately received intravenous hydrocortisone. Magnetic resonance imaging (MRI) of the pituitary showed a normal pituitary gland. Twenty-four hours after starting corticosteroid replacement, his symptoms and hyponatremia resolved. He was then switched from hydrocortisone to prednisolone. He was discharged on the 12th day of admission with prednisolone 7.5 mg/day and premixed insulin 26 U/day. Both his pembrolizumab and ipilimumab were discontinued due to IRAEs. Six months following hospital admission, he was seen in regular follow-up in the endocrinology department. His blood glucose levels were borderline controlled with premixed insulin 58 U/day. He remained on prednisone 7.5 mg/day, and he felt extremely fatigued if he missed a dose of prednisolone. He had stable disease even after ICI discontinuation and no further treatment.