Moreover, the combination of some drugs with lower TAC dose may be safely coadministered. However, our results provided evidence that CYP3A5 plays a more dominant role than other genetic variants in the metabolism of TAC in pediatric liver transplant recipients and their donors. In this study, we analyzed the relationship of pairing of donors and recipients. Among pairing of donors and recipients, parental relationship cases were more than grandparental those. In addition, there were not significantly different in occurrence of rejection between the same or different genotypes in pairing of donors and recipients. In additional, not only donors but also recipients were genotyped with their peripheral blood samples. It seems no difference for genotyping regardless of basing on intestinal biopsies or blood samples, but using intestinal biopsies will have high novelty, especially for recipients. More importantly, intestinal biopsies from recipients will provide us more valued information about mRNA transcription and protein expression of interesting genes and second pass of metabolism of TAC. The main limitations of this study are the retrospective design from a single center and a limited number of patients. Also, the confounding effects of CYP3A4 with ABCB1 or ACE variants that may affect TAC pharmacokinetics were not examined. A prospective study with a large number of pediatric recipients and standard timing of ImmuKnow assay is required to establish an effective monitoring tool of immune response in children following liver transplantation. Furthermore, for recipient genotyping, periphery blood has limited novelty. Both large and small animal species deficient for dystrophin have been described and have been extremely useful for preclinical studies of DMD. Although they display more features of the human clinical phenotype than mdx mice, large dystrophindeficient animals such as dogs and pigs, suffer from individual variability and are costly and time consuming. On the other hand, mdx mice exhibit only minor clinical dysfunction and their small size imposes limitations in the analysis of several aspects of the disease. Although each animal model has its own limitations, they have all been essential for the development of treatment strategies that target dystrophin absence, disease progression or muscle regeneration. Nevertheless, new animal models are needed to help pre-clinical research on DMD. We hypothesized that the rat could represent a useful model of DMD. One of its advantages of over mice is that its behavior is much better characterized. Rats have finer and more accurate motor coordination than mice and exhibit a richer behavioral display, including more complex social traits.