These findings are not inconsistent with our results. There are several limitations to our study. Overall, the sample size is not large enough to detect significant differences of minor VDR polymorphisms or synergistic effects of the gene-environment and stratification by tumor stage or primary site. Although FokI TT was a significant factor, the number was only 17 and 95%CI was sometimes wide. However, when we set number of patients as 175 FokI CC+CT vs. 19 FokI TT polymorphisms, Cetylpyridinium chloride monohydrate post-hoc power calculations showed 98% along with a hazard ratio of 2.73. Moreover, we did not use restriction fragment length polymorphism analysis and directly sequenced PCR fragments to avoid misclassification as much as possible and to compensate for the disadvantage of the small sample size. No information was available regarding vitamin D intake, sun exposure, or circulating vitamin D levels of patients. Moreover, we did not have clinical information on alcohol use, human papilloma virus, or Epstein-Barr virus infection. There are other kinds of VDR polymorphisms related to disease risks that have been reported in previous articles, and we need to expand our range of analysis in the future. In conclusion, there were significant associations between shorter progression-free survival time in patients with HNSCC and FokI T/T genotype as well as A-T-G haplotype, although the sample size is not large enough to detect significant differences of minor VDR polymorphisms or synergistic effects of the gene-environment and stratification by tumor stage or primary site. Recent research has shown that symptoms related to attentiondeficit hyperactivity disorder, a disorder predominantly linked to changes in catecholaminergic neurotransmission, are also affected by variation in serotonin-related genes. There is a considerable body of evidence showing that neurobiological and environmental factors significantly contribute to disorders and phenotypes associated with aggression and impulsivity. The neurotransmitter serotonin has been linked to the neurobiological underpinnings of aggressive behavior by a considerable body of animal research, suggesting that low central nervous system 5-HT activity is associated with aggression and impulsivity. A considerable amount of studies investigated the effects of changes in serotonergic Doxercalciferol neurotransmission on aggression in rodents. Evidence suggests that reduced serotonin-mediated inhibition facilitates aggressive behavior. Moreover, prolonged TRP deprivation lead to increased killing of mice in rats when compared to standard foods that were administered to the animals. However, the data of this particular study also suggested that mouse-killing persisted after rats were returned to standard food, indicating that reduced serotonergic neurotransmission did not influence the maintenance of aggression. In addition, research using the selective and irreversible TPH2 inhibitor p-chlorophenylalanine indicated.