Recent GWA studies have also identified risk loci in members of SLCs, such as SLC24A4.[9] Specific implication of SLC26A7 has also been shown through gene co-expression network mining where STAT1, a transcription factor of SLC26A7, was differentially expressed between AD patients and cognitively normal controls.[47] In our analysis, we identified nine rare deleterious SNVs in HLA-A in which six were predicted to be damaging missense mutations, two were predicted to be splice acceptor variants, and one was predicted to be either damaging missense mutation or splice region variant. This evidence concerns the gene HLA-A and Alzheimer disease.