A 35 year old man with Familial Mediterranean Fever (FMF) complicated by renal amyloidosis s/p renal transplant and diffuse large B-cell lymphoma was admitted for dialysis. Over 1 week, he had melena with downtrending hemoglobin (Hgb). Notably, EGD performed 3 months prior for abdominal pain showed gastritis and duodenal lymphocytosis on pathology. On presentation, push enteroscopy found a nonbleeding esophageal ulcer, erythematous gastric and nodular friable duodenal and jejunal mucosa. After BRBPR with an acute Hgb drop, interventional radiology performed angiography of mesenteric vessels but did not identify a bleeding source. After an episode of hematemesis, a second EGD showed visible vessels at the GE junction and in a gastric ulcer without intervention. Repeat EGD done 4 hours later for persistent bleeding showed GE junction and gastric incisura bleeding nodules that oozed despite APC. Pathology of EGD biopsies demonstrated amyloid with positive Congo red stain and immunostain for serum amyloid A (SAA). The patient's GI bleeding was attributed to gastric amyloidosis due to FMF. Surgery recommended a subtotal gastrectomy, but the patient deferred. However, after massive hematemesis, he underwent emergent surgery. Pathology revealed several hemorrhagic ulcers with gastric and duodenal amyloidosis of small vessels and lamina propria with gastric mucosal infarction. The patient died on day 39 due to persistent melena and sepsis with multiorgan failure. Defined as the extracellular deposition of abnormal protein, amyloid is categorized as primary, secondary, hemodialysis-related, hereditary, senile, and localized. This patient had secondary (AA) gastric and duodenal amyloidosis due to SAA deposition. AA amyloidosis is associated with inflammatory diseases, like FMF. Of patients with amyloidosis, 8% have gastric involvement. Endoscopic findings include thickened and irregular gastric folds, gastric ulcerations, and hematomas from amyloid deposits in submucosal vessels. The lamina propria was infiltrated by AA amyloid in 100% of gastric amyloid cases. Massive bleeding in GI amyloidosis is due to mucosal oozing, ulcers, and vascular fragility. Managing systemic amyloidosis requires treatment of the primary inflammatory disorder. Arterial embolization and surgery have been used, but reports of endoscopic hemostasis are lacking. Our case highlights the challenge of managing GI bleeding from amyloid and suggests that surgery should be considered early in the course.