Patients with known cirrhosis who present with anemia, thrombocytopenia, acute renal failure, and confusion are usually presenting with decompensated cirrhosis. We present a patient with known alcoholic cirrhosis presenting with the above abnormalities, initially thought to be decompensated cirrhosis but found to have acute myeloid leukemia (AML) with acute blast crisis. This case was presented as a poster at the American College of Gastroenterology Annual Scientific Meeting held on October 22-27, 2021. A 59-year-old male with a history of compensated alcoholic cirrhosis presented with unresponsiveness. On physical exam, vitals were normal, he appeared lethargic with generalized pallor, and rectal exam demonstrated an empty rectal vault with no blood or stool noted. Labs were notable for hemoglobin 3.1 g/dL, platelet count 41,000/µL, creatinine 5.2mg/dL, aspartate aminotransferase (AST) 242 U/L, alanine aminotransferase (ALT) 138 U/L, bilirubin 0.8 mg/dL, lactic acid 8.5 mmol/L, international normalized ratio (INR) 1.8, ammonia 51µmol/L. Imaging with CT head was unremarkable and CT abdomen demonstrated cirrhotic morphology of the liver with a small amount of ascites. Upper endoscopy was performed with no evidence of varices. Paracentesis demonstrated a high serum-ascites albumin gradient with low total protein consistent with portal hypertension. He was intubated for airway protection due to worsening encephalopathy. A peripheral smear was performed which showed myeloblasts with no signs of hemolysis. Bone marrow biopsy was subsequently performed which revealed 38% myeloblasts and features of myelodysplastic syndrome suggestive of secondary AML. Chemotherapy was not initiated as he was acutely critically ill and he expired shortly thereafter. AML can present with symptomatic anemia, bleeding, mental status changes due to central nervous system involvement, organomegaly, and renal insufficiency. Diagnosing AML in the setting of decompensated liver cirrhosis can be difficult as the clinical presentations can be similar at times. Thus, hematological causes should be considered when there is profound anemia with no acute blood loss early in the course.