Introduction: Amyloidosis is extracellular tissue deposition of fibrils with either localized or systemic involvement. We describe a case of a 49 year female who presented with persistent epigastric abdominal pain diagnosed with gastric amyloidosis on gastric biopsies. Case report: A 49 year old female with multiple comorbidities including multiple myeloma s/p chemotherapy and tandem auto stem cell transplant, AL amyloidosis, hypothyroidism, hypertension, DVT presented to the clinic for worsening epigastric pain, nausea and early satiety for the past 4-5 months. Patient has been admitted thrice for similar complaints. During previous admissions, lab revealed thrombocytopenia with platelets 12K, Hb/Hct 9/27, total protein 6.8, ALP 337, SGOT 102 and SGPT 64. Patient was found to be in fluid overload with ECHO showing EF 50%; sono abdomen showed normal gallbladder with wall thickening, calculus and enlarged liver. Upper endoscopy 2 years back showed mild gastritis. Hence her symptoms were attributed to congestive hepatopathy vs cholecystitis/ peptic ulceration. In spite of interventions, patient symptoms got worse she underwent an upper endoscopy and biopsies revealed rare small capillaries with deposition of amyloid within stomach wall diagnosed with gastric amyloidosis. Her symptoms were attributed to autonomic neuropathy as a result of amyloidosis. Discussion: Amyloidosis is classified as primary (AL) or secondary (AA) amyloidosis. Gastrointestinal disease is present in as many as 60 percent of patients with AA amyloidosis and appears to be less common in AL amyloidosis. Gastric amyloidosis can present with symptoms secondary to direct involvement of GI tract or deposition of amyloid within the autonomic nervous system. Infiltration of stomach causes gastric outlet obstruction, ulcers or bleeding whereas amyloid deposition in small bowel leads to malabsorption, pseudoobstruction, intestinal dysmotility and protein losing enteropathy. Delayed gastric emptying may result from infiltration of autonomic nerve and/or smooth-muscle. On endoscopy, AL amyloidosis appears as polypoid mass lesion whereas AA amyloidosis have fine granular appearance, mucosal friability, and erosions. The diagnosis requires a tissue biopsy with positive staining of amyloid by Congo red or the presence of amyloid fibrils on electron microscopy. The mainstay treatment for AL amyloidosis has been chemotherapy though it carries a poor prognosis despite treatment. Metoclopramide is useful in supportive treatment of gastroparesis caused by amyloidosis. Our case is unique as patient has AL amyloidosis with GI tract involvement. Initially was thought to have symptoms due to cardiac causes, ultimately diagnosed with gastric amyloidosis causing gastroparesis.