One study has shown a correlation between the SNP of SLCO3A1 and QT prolongation in schizophrenic patients treated with iloperidone. Schizophrenia is known to be associated with a high prevalence of smoking. Meta-analyses of GWAS have also shown that SLCO3A1 is associated with nicotine dependence. As shown in a previous study, nicotine increases oxidative stress, activates NF-kB, and induces apoptosis. In our study, we have provided evidence that nicotine induction leads to enhanced NF-kB activation in the presence of SLCO3A1. These findings are consistent with the hypothesis that smoking exacerbates the course of CD due to allelic change of SLCO3A1. We are aware of limitations associated with this study due to the small sample size. As emphasized in the introduction, CD is still a low incidence/prevalence disease in Taiwan. Therefore, despite our best efforts to enroll patients, the sample size was small. We would like to see further validation of these results from other countries in the future. Secondly, the tissues used for control were not ideal. Theoretically, age-and sex-matched healthy individuals and subjects with non-IBD inflammationwould be more appropriate for the control group. However, in clinical practice, these conditions are not appropriate or indicated for endoscopy or surgery. Therefore, we were not able to obtain this Ergosterol tissue for use as control. Instead, we used colorectal cancer and intestine transplantation tissue since these are Gomisin-D obtainable in clinical practice. The gender ratio of colorectal cancer is similar to that of IBD in Taiwan. With respect to age, we performed a correlation analysis of the expression of SLCO3A1 and age, and found no correlation between them. Therefore, we concluded that it would be acceptable to use the current control for interpreting the results. In conclusion, SLCO3A1 is a novel CD-associated gene based on our Illumina platform analysis and functional study results. Expression of SLCO3A1 activates the NF-kB transcription factor mediating inflammatory processes, consequently inducing increased activation of ERK and JNK phosphorylation and leading to a more intense and protracted NF-kB activation in intestinal epithelial cells. Active disease CD tissue expressed higher levels of SLCO3A1 compared with tissue analyzed from patients in remission. Stronger inflammation is associated with a greater chance of a perforated CD phenotype. Nicotine enhances the NFkB activation in the presence of SLCO3A1, which can partially explain smoking’s influence as an aggravating factor for CD. The atmospheric oxidation of group 13 metal alkyls is usually very rapid and uncontrollable, often resulting in combustion.However, controlled oxidation by limited exposure to oxygen gas results in the production of organoperoxide compounds, or alkoxide compounds through the decomposition of the former.It has been well established that the formation of the alkoxide occurs through an intermolecular oxygen transfer, not an intramolecular one.Thus, it is possible to isolate stable complexes bearing a strongly reducing metal-alkyl bond in close proximity of a strongly oxidizing metal-peroxide bond.However, it was demonstrated that spatial requirement plays an important part in the oxidation of group 13 metal alkyls. Recently I became interested in pursuing complexes that bear resemblance to methylalumoxane, a common co-catalyst.