FKBP1A and diabetic ketoacidosis: TAC and cyclosporin have been reported to cause post-transplant diabetes.[1] The diabetogenic potential of TAC is considered to involve suppression of insulin secretion from pancreatic beta cells by inhibiting transcription of the insulin gene, due to the association between TAC and the FK506-binding protein 12 (FKBP-12).[2] Although some cases of TAC-related diabetic ketoacidosis (DKA) have been reported,[1,3] few cases have involved changes in insulin secretion before and after TAC cessation.