The case was a 57-year-old man who presented with abnormal shadows in the left upper lung field on a chest radiograph that was taken during a routine health examination (Fig. 1-A). He had a history of dyslipidemia, which was not treated with medications. Computed tomography (CT) of the chest showed a lung nodule measuring 28 x 20 mm in the left upper lobe. A transbronchial lung biopsy was performed, and the nodule specimen consisted of a granuloma with necrosis. On Ziehl-Neelsen stain, the sputum, bronchial lavage, and nodule specimen were negative. After 6 weeks, the bronchial lavage culture yielded Mycobacterium tuberculosis. Therefore, we made the diagnosis of mycobacterium tuberculoma, and treated the patient with INH (0.3 g/day), rifampicin (RFP) (0.45 g/day), ethambutol (EB) (0.75 g/day), and pyrazinamide (PZA) (1.2 g/day). Three weeks later, he developed fever, headache, and appetite loss. On physical examination, body temperature was 39.1  C, blood pressure was 96/64 mmHg, pulse rate was 112 beats/min, and percutaneous oxygen saturation (SpO2) on room air was 96%. Chest examination was normal, and no lymph nodes were palpable. At this time, a chest radiograph showed diffuse micronodular shadows in both lung fields (Fig. 1-B) and on high-resolution CT (HRCT) of the chest there were diffuse numerous parenchymal micronodules in both lungs such as in hypersensitivity pneumonia (Fig. 2). He was admitted for further evaluation. The white blood cell (WBC) count was elevated to 8700/mul with 67.9% neutrophils, 12.6% lymphocytes, 12.1% monocytes, 6.5% eosinophils, and 0.9% basophils. C-reactive protein and lactate dehydrogenase (LDH) were also elevated to 10.4 mg/dl and 243 IU/l. Other laboratory data including those for liver function, renal function, electrolytes, KL-6 (179 U/ml), and surfactant protein-D (104 ng/ml) were within normal range. Cultures of sputum, urine, and blood showed no growth. We suspected drug-induced pneumonia and stopped the antituberculous drugs, after which his symptoms and diffuse micronodular shadows on chest radiograph and HRCT (Fig. 3, Fig. 4B) rapidly improved without any medication, including corticosteroid. A drug lymphocyte stimulation test (DLST) on a serum sample was performed. As a result, only INH was positive with an increase in the [3H]-thymidine uptake by 219% (normal < 180%), while RFP (112%), EB (90%), and PZA (98%) were negative. Based on this result, we concluded that the pneumonia was induced by INH. Ten days after the cessation of the antituberculous drugs, the patient was discharged. Two weeks after discontinuing the antituberculous drugs, PZA (1.2 g/day) was reintroduced. Although the abnormal shadows and symptoms did not return, liver dysfunction developed, and PZA was discontinued again. Since liver function recovered to normal by only stopping PZA, RFP (0.45 g/day) was reintroduced one week after discontinuing PZA, and EB (0.75 g/day) was reintroduced two weeks after discontinuing PZA. Next, we attempted desensitization to INH over a period of two weeks. The regimen for desensitization was as follows: days 1-3 25 mg/day, days 4-6 50 mg/day, days 7-9 100 mg/day, days 10-12 200 mg/day, and days 13 and 14 300 mg/day. Desensitization to INH was successful, and RFP, EB, and INH were given for 9 months without any adverse events, including recurrence of the abnormal shadows on the chest radiographs and HRCT (Fig. 3, Fig. 4C).