In addition, serum resistin probably exists as a Delsoline hexamer or trimer in mice. The presence of multimers in human serum has been suggested, and this may also have affected the assay results. In summary, of the potentially Thiacetazone functional SNPs, SNP-358 appears to be most strongly associated with plasma resistin in the general Japanese population, followed by SNP-420. Subjects having the responsible allele for the highest plasma resistin, A at 2358, generally had G at 2420. The G-A haplotype defined by SNP-420 and SNP-358 conferred the highest plasma resistin. Functionally, the RETN promoter with this G-A haplotype showed the highest activity. It is not clear why A of SNP-358 is required for G of SNP-420 to confer the highest plasma resistin, and whether the A of SNP-358 indeed accounts for ethnic differences in the association between plasma resistin and SNP-420. Further studies will be required to clarify these points. High-level microsatellite instability is the molecular hallmark of a subset of colorectal cancers which carry defects in DNA mismatch repair. MSI is defined as nucleotide length abnormalities occurring within short DNA sequences consisting of iterated oligonucleotide units, and is widespread throughout the genomes of MSI-H CRC. MSI exerts its tumorigenic effects when it occurs within protein coding regions thereby disabling tumor suppressor genes in MSI-H CRCs via frameshift mutation. The genome-wide distributions of these coding MSI events have been studied extensively in different tumor types by several groups, including our own. MSI also occurs within the 39-untranslated regions of genes. Recent advances in RNA research have revealed that the 39UTR plays a prominent role in regulating the stability, subcellular localization, and translation of its parent mRNA via sequence-specific interactions with trans-acting factors including small RNAs and proteins. Mutations within the 39UTR can affect gene activity if they alter RNA sequence or structure relevant to these interactions. Several 39UTR point mutations have been linked to the risk of developing cancer in humans. Recent reports have also shown that deleterious mutations at two 39UTR mononucleotide repeats destabilize the mRNAs in which these mutations occur.