A 52-year-old African American male was admitted to the hospital for high-dose chemotherapy for refractory aggressive multiple myeloma (MM). He had previously progressed through bortezomib/dexamethasone and lenalidomide therapy. The most recent bone marrow biopsy showed approximately 90% kappa light chain-restricted plasma cells with a high proliferative rate (3.3% cells in S-phase). Admission labs prior to starting any therapy (Table I) were significant for uric acid 16.1 mg/ dL (reference range, 3.7-8.0), creatinine 2.1 mg/dL (reference range, 0.8-1.3 and his baseline was 1.1), lactate dehydrogenase (LDH) 438 U/L (reference range, 122-222), phosphorus 6.2 mg/dL (reference range, 2.5-4.5), hemoglobin 7.1 g/dL (reference range, 13.5-17.5), and IgG kappa monoclonal protein of 4.1 g/dL. On admission, baseline pulse oximetry at the bedside was normal at 95% O 2 saturation (SpO2). Due to baseline renal insufficiency and anticipated tumor lysis, intravenous (IV) fluids were started immediately followed by 6 mg of rasburicase on Day 1. High-dose IV cyclophosphamide (1,500 mg/m 2 ) and 1,000 mg of methylprednisolone were administered in the early morning on Day 2.This patient presents with hyperuricemia and hyperphosphatemia with laboratory levels that meet Cairo-Bishop criteria of tumor lysis syndrome (TLS) even before chemotherapy was initiated [1,2]. In addition, he also has an acute kidney injury (AKI) secondary to TLS occurring in the setting of refractory MM as manifested by high tumor burden, high plasma cell proliferative rate, increased serum LDH, and a very high uric acid with AKI.Given the clinical features and baseline hyperuricemia and AKI, rasburicase should be administered to prevent worsening renal failure. A glucose-6-phosphatase dehydrogenase (G6PD) level is usually obtained in patients receiving rasburicase because rasburicase can induce hemolysis and cause methemoglobinemia in enzyme-deficient individuals. In our patient, the options were to give rasburicase or to provide prophylactic kidney dialysis without rasburicase. We proceeded with rasburicase given the need for immediate chemotherapy.On hospital Day 2, bedside pulse oximetry showed significant hypoxemia (SpO2 75%), triggering an emergency consultation with the critical care team. The patient was evaluated and found to be quite comfortable on room air with a respiratory rate of 16 per minute without the use of accessory muscles of respiration; lung, cardiac, and mucous membrane examinations were normal. An arterial blood gas (ABG) was performed and the arterial blood was noted to be brown in color. ABG showed pH 7.39, pO 2 104 mmHg, pCO 2 39 mmHg, HCO 3 24 mmol/L and methemoglobin 12.9% (normal range, 0-1.5%). At this point, the care team discussed the use of IV methylene blue.