A 70-year-old woman complained of low-grade fever (37.5 °C), general fatigue, loss of appetite for 2 d, and nausea and watery diarrhea beginning on day 11 (with day 1 being the day on which chemotherapy was started). Four months ago, she had developed ALL and achieved complete remission (CR) with induction chemotherapy. She received consolidation chemotherapy with cytarabine (1.4 g, 2 times/d), etoposide (100 mg/d) and dexamethasone (33 mg/d) for 3 d. On the first day (day 1), intrathecal injection of methotrexate (15 mg), cytarabine (40 mg) and prednisolone (10 mg) was also administered. The white blood cell count (WBC) began to decrease steadily, and on day 7, a granulocyte-colony stimulating factor (G-CSF) preparation (lenograstim) was used, but the decline continued. She was on medication for dyslipidemia and gastroesophageal reflux disease. For the latter, she was taking vonoprazan (10 mg) before she developed the present disease. There was no personal and family history. On day 11, she exhibited the following vital signs that were consistent with septic shock: body temperature increase to 38.1 °C; temporary drop in blood pressure to 78/60 mmHg; heart rate of 126 beats/min; respiratory rate of 31 breaths/min; and pulse oximetry (SpO2) of 96%. She was obviously sick and was lying down, but there was no apparent loss of consciousness. Physical examination revealed mild tenderness in the upper abdomen. The venous blood culture was later found to reveal the presence of Bacillus cereus. The culture of the tip of the removed central venous catheter was negative. The other data on day 11 to day 17 are shown in Table. WBC had decreased to 100/μL on day 11 (also shown in Figure ). C-reactive protein (CRP) levels increased rapidly to 29.71 mg/dL on day 11 and to 46.82 mg/dL on day 13. WBC markedly increased to 45000/μL on day 15 and 66000/μL on day 17 despite stopping G-CSF. Liver dysfunction was observed in conjunction with elevated WBC. An abdominal computed tomography (CT) scan on day 11 showed marked thickening of the gastric wall. CT also showed findings suggestive of HPVG scattered in the liver; in addition, low-density areas (LDAs) were found in liver S3 and S7. Esophagogastroduodenoscopy (EGD) on day 14 showed marked thickening of the gastric wall in the corpus of the stomach as well as yellow-green pseudomembrane-like tissue covering the superficial mucosa. This patient was clinically diagnosed with PG with HPVG. EGD on day 29 revealed that the abovementioned abnormal findings improved in 15 d, and linear redness, erosion and ulcerative mucosal changes were observed. On the same day, CT showed improvements in thickening of the gastric wall, and the findings suggestive of HPVG disappeared. In addition, LDAs in liver S3 and S7 originally observed on day 11 changed to findings consistent with abscesses.