{{Rsnum
|rsid=1670283
|Gene=ALK
|Chromosome=2
|position=29193706
|Orientation=plus
|ReferenceAllele=A
|MissenseAllele=G
|GMAF=0.006887
|Assembly=GRCh38
|GenomeBuild=38.1
|dbSNPBuild=141
|geno1=(C;C)
|geno2=(C;T)
|geno3=(T;T)
|Gene_s=ALK
}}{{ population diversity
| geno1=(C;C)
| geno2=(C;T)
| geno3=(T;T)
| CEU | 100.0 | 0.0 | 0.0
| HCB | 100.0 | 0.0 | 0.0
| JPT | 100.0 | 0.0 | 0.0
| YRI | 92.4 | 7.6 | 0.0
| ASW | 93.0 | 7.0 | 0.0
| CHB | 100.0 | 0.0 | 0.0
| CHD | 0.0 | 0.0 | 0.0
| GIH | 0.0 | 0.0 | 0.0
| LWK | 96.3 | 3.7 | 0.0
| MEX | 0.0 | 0.0 | 0.0
| MKK | 98.1 | 1.9 | 0.0
| TSI | 0.0 | 0.0 | 0.0
| HapMapRevision=28
}}{{Venter SNP
|rsid=1670283
|allele=C
|frequency=1
|uid=1103658054085
|type=homozygous_SNP
|hugo=ALK
|ensembl gene=ENSG00000171094
|ensembl transcript=ENST00000306036
|sift=TOLERATED
|disease=A chromosomal aberration involving ALK is found in a form of non-Hodgkin lymphoma. Translocation t(2;5)(p23;q35) with NPM1. The resulting chimeric NPM1-ALK protein homodimerize and the kinase becomes constitutively activated. The constitutively active fusion proteins are responsible for 5-10% of non-Hodgkin lymphomas.
}}

{{GET Evidence
|gene=ALK
|aa_change=Ile1461Val
|aa_change_short=I1461V
|impact=not reviewed
|qualified_impact=Insufficiently evaluated not reviewed
|inheritance=unknown
|quality_scores=Array
|dbsnp_id=rs1670283
|overall_frequency_n=10640
|overall_frequency_d=10758
|overall_frequency=0.989031
|n_genomes=56
|n_genomes_annotated=0
|n_haplomes=110
|n_articles=0
|n_articles_annotated=0
|qualityscore_in_silico=2
|qualitycomment_in_silico=Y
|gene_in_genetests=Y
|genetests_testable=Y
|genetests_reviewed=Y
|nblosum100=-4
|autoscore=3
|n_web_uneval=1
}}

{{on chip | Affy GenomeWide 6}}
{{on chip | FTDNA2}}
{{on chip | HumanOmni1Quad}}
{{on chip | Illumina Human 1M}}