 Tacrolimus is metabolized through the liver by the cytochrome P450 system, the cytochrome P450 3A5 CYP 3A5 isoenzyme specifically. Polymorphisms in the CYP 3A5 gene have been associated with changes in metabolic function of the translated isoenzyme. These polymorphisms result in metabolism acceleration of tacrolimus as compared to subjects having the wild type gene, consequently leading to insufficiency of tacrolimus; it is theorized that this leads to higher risk of acute rejection. Several retrospective studies suggested an association between a genetic polymorphism of CYP3A5 and the interindividual variations of tacrolimus blood concentration. In particular, our initial study showed that adult renal transplant recipients with the CYP3A513 and 11 expressors genotype require higher, fixed, starting dose compared with CYP3A533 nonexpressorto reach the predefined target exposure early after transplantation. 