Acute pancreatitisis is a well described complication of L-asparaginase therapy [1,3]. Complications include hemorrhage, pseudocyst formation, pancreatic insufficiency, sepsis, and respiratory distress due to pulmonary edema or pleural effusion [2,5]. An 8 year old boy with ALL, who was on St. Jude Total XIII-high risk continuation therapy, tolerated E-coli asparaginase treatments well until he developed anaphylaxis reaction during E-coli asparaginase administration at 8 th week of continuation therapy. According to protocol the next L-asparaginase treatment was four weeks later. We switched E-coli asparaginase to Erwinia asparaginase, and he received vincristine, and prednisone at the 12 th week of continuation treatment. One week after first Erwinia asparaginase administration the patient was admitted to hospital with vomiting, diffuse abdominal pain and decreased oral intake. Physical examination revealed a pale, ill appearing child in acute distress with a diffuse sensitivity of upper abdomen but no rebound tenderness or guarding. Laboratory findings showed an amylase level of 477 mg/dl (normal <125 mg/dl), pancreatic lipase 292 U/L (0-60 U/L), pancreatic amylase 81 U/L (17-115 U/L). The most possible diagnosis was drug induced pancreatitis. Repeated laboratory evaluation showed a gradual increase in the serum amylase to 775 mg/dl by hospital day two. On the second day of admission, ultrasonography of the abdomen showed the pancreas was diffusely enlarged and heteroechogen. Although hypoechoic texture is expected in pancreatitis, ultrasonographic evaluation was heteroechogen in our patient. On the third day of admission abdominal computed tomography (CT) study was done to explain heteroechogenity in ultrasonography. Computed tomography scanning with intravenous contrast