{{Rsnum
|rsid=1186868
|Chromosome=2
|position=61764103
|Orientation=plus
|GMAF=0.05556
|Assembly=GRCh38
|GenomeBuild=38.1
|dbSNPBuild=141
|geno1=(A;A)
|geno2=(A;G)
|geno3=(G;G)
}}{{GWAS Summary
|SNP=rs1186868
|PubMedID=18245381
|Condition=Fetal hemoglobin levels
|Gene=BCL11A
|Risk Allele=T
|pValue=7.00E-035
|OR=0.48
|95CI=NR) SD decrease in Hb
|OA=1
}}

{{PharmGKB
|RSID=rs1186868
|Name_s=
|Gene_s=-
|Feature=
|Evidence=PubMed ID:18245381; Web Resource:http://www.genome.gov/gwastudies/
|Annotation=GWAS Results: Genome-wide association study shows BCL11A associated with persistent fetal hemoglobin and amelioration of the phenotype of beta-thalassemia (Initial Sample Size: 4,305 individuals; Replication Sample Size: 521 individuals; Risk Allele: rs1186868-T).
|Drugs=
|Drug Classes=
|Diseases=
|Curation Level=Non-Curated
|PharmGKB Accession ID=PA162356738
}}

{{PMID|19474294|OA=1
}} Potential etiologic and functional implications of genome-wide association loci for human diseases and traits.

{{GET Evidence
|impact=pathogenic
|qualified_impact=Insufficiently evaluated pathogenic
|inheritance=unknown
|quality_scores=Array
|dbsnp_id=rs1186868
|overall_frequency_n=4
|overall_frequency_d=128
|overall_frequency=0.03125
|n_genomes=5
|n_genomes_annotated=0
|n_haplomes=5
|n_articles=0
|n_articles_annotated=0
|in_gwas=Y
|in_pharmgkb=Y
|autoscore=2
|webscore=N
|n_web_uneval=7
}}

{{on chip | 23andMe v3}}
{{on chip | 23andMe v4}}
{{on chip | FTDNA2}}
{{on chip | FTDNA}}
{{on chip | HumanOmni1Quad}}