Since methylation Ganoderic-acid-G status of PCGI and NPNCGI was inversely correlated, positive correlation between NPNCGI methylation and SLC6A4 mRNA level seems to be reasonable. On the other hand, DNA methylation in NPNCGI has been also thought to have influence on gene expression through transcriptional factor binding. The NPNCGI in the SLC6A4, analyzed in this study have numerous transcriptional factor binding sites but the role of these transcriptional factors in FD seemed to be unclear. Therefore whether the methylation change of SLC6A4 NPNCGI would be a cause or consequence of other regulatory mechanisms needs to be Ergosterol investigated. SERT signaling plays an important role for braingut communication and functional gastrointestinal disorders. Several reports have demonstrated that genetic polymorphism SLC6A4, affecting 5-HTT expression level is associated with susceptibility to functional gastrointestinal disorders. Together with the comparison of methylation status among FD and control, our result suggests that epigenetic alteration of SLC6A4, leading to higher mRNA level may be associated with subset of FD. We have also shown that lower methylation level in PNCGIs, respectively. These associations indicate that different FD subgroups have different molecular backgrounds. FD is so diverse in its symptom, clinical course and response to treatment and this heterogeneity is explained by complex pathophysiologic mechanisms, which is not conclusive. Our result suggest that low methylation level 
in PNCGIs and high methylation level in NPNCGIs would be useful molecular marker in PDS and EPS, respectively. In addition, association between methylation level of SLC6A4 with specific subtypes of FD suggest that different epigenetic status of SLC6A4 may one of the explanation of heterogeneity of FD, which needs to be mechanistically clarified. Our data demonstrated that, although significant, differences of SLC6A4 methylation status seen in this study are mostly small with large overlap between cases and controls, suggesting the pathogenic role of SLC6A4 methylation status only in a subset of FD patients. The small sample size and marginal statistical difference could not obtain strong statistical power, which should be addressed as the limitation of our study. Since this is the first reporting the potential role of epigenetics in the development of FD, further well designed study will be needed to confirm our finding. Mandibular defects can be caused by ablative surgery for oral and maxillofacial tumors, trauma, infection, or congenital deformities. The reconstruction of large mandibular defects is a highly challenging task for oral and maxillofacial surgeons. Despite the many reconstructive methods available, autologous grafts are considered to be the “gold standard” because of their advantages of osteogenesis, osteoinduction, and osteoconduction. The iliac crest is the most frequently chosen donor site because it provides easy access to good-quality cancellous autografts in appreciable numbers. However, harvesting autologous bone from the iliac crest lengthens the overall surgical procedure and is usually complicated by hematoma formation, pelvic instability, nerve injury, residual pain, and cosmetic disadvantages. Also, the shape of the mandible reconstructed by autogenous bone grafts is poor. Hence, a better method for mandibular reconstruction is required. As the number of bone banks has increased, so has the number of bone allografts used in reconstructive surgery to replace missing bone parts.