A 34 year old female with chronic kidney disease secondary to DM-i underwent an HLA identical living donor kidney transplant with a weakly positive flow cytometric crossmatch (FCXM), but without any donor specific antibody (DSA) [Table1]. Crossmatch became progressively more positive with time, but without detectable DSA. Tests to detect non-HLA antibody and autoantibody were negative. Allograft function was good, protocol biopsies did not show any rejection. She later received a pancreas allograft, again with a weakly positive FCXM, without DSA. The pancreas functioned well until about 6 weeks posttransplant when she developed hyperglycemia. Cross-sectional imaging demonstrated non-enhancing pancreas allograft with new vein thrombosis. She underwent transplant pancreatectomy of the non-viable, necrotic graft. Pathology demonstrated massive parenchymal necrosis, numerous intravascular thrombi, inflammation of the viable pancreas with C4d deposition in the vessels. She had also developed several de-novo class-I DSAs at this time [Table2]. This is consistent with severe acute antibody mediated rejection (AMR) of the pancreas leading to venous thrombosis and graft necrosis. Despite extensive testing, we were not able to identify a causative antibody for the initial positive FCXMs or its role in the eventual rejection of the pancreas allograft.