A 65-year-old man underwent radical esophagectomy 5 months ago following the diagnosis of esophageal cancer by gastroscopy. The postoperative pathology was well-differentiated squamous cell carcinoma of the esophagus, involving the adventitia and local foci around the esophagus. Approximately 40 days later, mediastinal lymph node metastasis was observed. Capecitabine was administered at a dosage of 1.5 g per os, twice daily for 14 days. At that time, the patient's liver and kidney function tests were normal, and 1 week later, an anti-programmed death-ligand 1 agent (camrelizumab 200 mg) was administered twice with a 2-week interval between each dose. Around 20 days later, abnormal liver function was detected: total bilirubin (TBIL), 52.2 micromol/L; direct bilirubin (DBIL), 38.8 micromol/L; alanine aminotransferase (ALT), 176.7 U/L; aspartate aminotransferase (AST), 250.5 U/L; alkaline phosphatase (ALP), 336 U/L; and gamma-glutamyl transpeptidase (GGT), 638 U/L. He received a diagnosis of drug-induced liver injury (DILI). Approximately 1 week later, his ALT and AST levels decreased rapidly, and TBIL continued to deteriorate (Figure 1). Considering the possibility of intrahepatic cholestasis, the physician added ursodeoxycholic acid (25 mg/kg/day) and methylprednisolone (20 mg/day). However, the cholestasis did not improve notably. Then, plasma exchange (PE) and a double plasma molecular absorption system (DPMAS) for blood purification were added, and cholestasis improved within a short time (Figure 1). During this period, except for yellow skin and dark urine, the patient had no other symptoms. Nonetheless, chest tightness and shortness of breath developed after 1 month of hospitalization. Chest computed tomography (CT) scanning revealed interstitial inflammatory lesions in both lower lungs (Figure 2). Liver biopsy revealed nonspecific immune injury (Figure 3). The doctor revised the diagnosis as immune-related pneumonia and hepatitis associated with camrelizumab. The treatment regimen of methylprednisolone was adjusted to 40 mg/day and gradually increased to 80 mg/day and mycophenolate mofetil 2 g/day was also added. Consequently, chest tightness and shortness of breath resolved, and pulmonary inflammation improved (Figure 2). Nevertheless, jaundice did not improve and continued to exacerbate. During the last 2 weeks of hospitalization, the patient showed symptoms such as high fever, decreased appetite, vomiting, and diarrhea. He was treated with human serum albumin (0.5-1.0 g/day), human hemoglobin (1.0-1.5 g/day), cefoperazone sulbactam (2 g, q12h), and caspofungin (50 mg). The last measured prothrombin time was 41 s, prothrombin activity was 19%, and the international normalized ratio was 4.03. The cause of death was diagnosed as liver failure, cardiopulmonary failure, and septic shock. The serum markers of hepatitis A-E were negative; nuclear antibody, mitochondrial antibody, liver, and kidney microsomal antibody, and anti-liver soluble antigen-antibody were negative; and immunoglobulin G value was 8.93 g/L (<16 g/L). Obstructive jaundice was excluded by multiple imaging examinations. Contrast-enhanced abdominal CT showed heterogeneous enhancement of liver density (Figure 4).