Neuronally expressed genes, which have been the central focus of functional studies regarding these and other AD risk genes, only represent 11% of IGAP GWAS loci: ABCA7, MADD, CELF1, and MEF2C. These findings provide further evidence of the complex interplay between genotype, expression, and cell-type that mediates AD risk. Here, CELF1 is linked to Alzheimer disease.