The 60-year-old male patient came to the chest diseases department of our hospital with the complaints of progressively increasing cough, dyspnea, and fatigue in the recent two years. The patient who denied hemoptysis said that he rarely produced sputum. He had no chronic disease except AS diagnosed in 1976. He never smoked. He had no alcohol consumption. He had no continuous medication except nonsteroid anti-inflammatory drugs (NSAIDs) for 2-3 days monthly since his pain of the musculoskeletal system decreased dramatically in the recent years. His physical examination revealed a blood pressure of 110/70 mmHg and 36.8 C body temperature. Heart beats were rhythmic, and no murmur was present. Breath sounds decreased in the upper zone of the right lung. The chest expansion and the lumbar Schober test measured 0 cm. Laboratory test results were found as follows: erythrocyte sedimentation rate (ESR) 72 mm/h, C-reactive protein (CRP) 28 mg/dL (normal range: 0-5), leukocytes 7800/mm3, hemoglobin 11 g/dL, platelets 323.000/mm3, and total protein/albumin ratio 6.8/3.3 g/dL. Other biochemical tests, electrolytes, and urinalysis results were within normal limits. Spirometric pulmonary function tests (PFT) revealed a restrictive pattern: a forced vital capacity (FVC) of 1.58 L (38% of predicted), a forced expiratory volume in 1 s (FEV1) of 1.50 L (46% of predicted), and an FEV1/FVC 94% and carbon monoxide diffusion capacity (DLCO) of 23 mL/min per mmHg (43% of predicted). Lung radiography revealed increased diffuse opacity in the upper zones of the right lung (Figure 1). Also, it showed right tracheal deviation and blunting of the right costophrenic sinus. Thoracic HRCT revealed the chronic consolidation with traction bronchiectasis compatible with fibrosis in the apical and posterior segments of the right upper lobe extending to the superior segment of the right lower lobe (Figure 2). In addition, there were also nodular alveolar densities in the lateral basal segment of the right lower lobe. Thoracic CT performed in 2016 showed mild bronchiectasis and sequela parenchymal bands in the middle lobe of the right lung. However, there was no apical fibrotic change, traction bronchiectasis, and parenchymal destruction in the upper lobe of the right lung (Figure 3). The comparison between thoracic HRCT and CT images suggested that pulmonary apical fibrosis and parenchymal destruction encountered in the right lung have developed in the recent three years. Gram staining, methylene blue stain, and Ehrlich-Ziehl-Neelsen (EZN) stain of the sputum revealed no pathogen, and all subsequent sputum cultures were negative. The tuberculin skin test resulted 0 mm, and the interferon-gamma release assay (IGRA) detected no Mycobacterium tuberculosis infection. Bronchoscopy and transbronchial lung biopsy were performed. Biopsy did not reveal any finding of malignancy, granulomatous inflammation, or vasculitis. Lumbar vertebral and pelvis X-ray revealed bilateral grade IV sacroiliitis, syndesmophytes, and appearance of "bamboo spine." As a conclusion, the patient was diagnosed with pulmonary involvement of AS including apical pleural thickening with upper lobe fibrosis and nonspecific interstitial abnormalities. Etanercept 50 mg/week and meloxicam 15 mg/day were administered. The patient was hospitalized for two weeks and included in the pulmonary rehabilitation programme. The next control examination after six weeks resulted as follows: ESR 36 mm/h, CRP 8 mg/dL, FVC of 41% of predicted, FEV1 of 49% of predicted, FEV1/FVC 96%, and DLCO 71% of predicted. After a six-month course of etanercept treatment, the patient did not develop new pulmonary lesion, and the drug was well tolerated without any adverse events.