{{Rsnum
|rsid=16888589
|Chromosome=8
|position=116623363
|Orientation=plus
|GMAF=0.07254
|Assembly=GRCh38
|GenomeBuild=38.1
|dbSNPBuild=141
|geno1=(A;A)
|geno2=(A;G)
|geno3=(G;G)
}}{{ population diversity
| geno1=(A;A)
| geno2=(A;G)
| geno3=(G;G)
| CEU | 79.6 | 20.4 | 0.0
| HCB | 99.3 | 0.7 | 0.0
| JPT | 100.0 | 0.0 | 0.0
| YRI | 72.8 | 25.2 | 2.0
| ASW | 84.2 | 14.0 | 1.8
| CHB | 99.3 | 0.7 | 0.0
| CHD | 0.0 | 0.0 | 0.0
| GIH | 84.2 | 15.8 | 0.0
| LWK | 83.6 | 15.5 | 0.9
| MEX | 91.4 | 6.9 | 1.7
| MKK | 82.1 | 14.7 | 3.2
| TSI | 87.3 | 11.8 | 1.0
| HapMapRevision=28
}}[[rs16888589]] is a SNP on ch 8q23 near the [[EIFH3]] gene, and it appears to be able to influence the amount of EIFH3 protein made.

[[rs16888589]] may have a causative role in increasing the risk for [[colorectal cancer]]; specifically, the minor (i.e. less frequent) [[rs16888589]](G) allele is associated with more EIFH3 protein, in turn associated with more cancerous cell growth and invasiveness. In a statistical sense, the [[rs16888589]](G) allele is associated with a 1.4 - 2 fold increase in risk. The authors of this study also conclude that several other nearby SNPs ([[rs16892766]] and [[rs11986063]]) that have been statistically linked to higher [[colorectal cancer]] risk are part of a tightly linked haplotype with [[rs16888589]], i.e. they are often inherited together, but these other SNPs are not likely to be causative since on their own in in vitro experiments they do not influence EIFH3 protein amounts.{{doi|10.1371/journal.pgen.1001126}}

{{PMID Auto
|PMID=21314996
|Title=Systematic search for enhancer elements and somatic allelic imbalance at seven low-penetrance colorectal cancer predisposition loci.
|OA=1
}}

{{on chip | Affy GenomeWide 6}}
{{on chip | FTDNA2}}
{{on chip | FTDNA}}