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Genome-wide association studies (GWASs) have changed the way we conceive human genetics and have led to the discovery of thousands of risk variants involved in disease etiology. However, despite tremendous advances made in understanding the genetic architecture underlying disease, there remains an underinvestigated component of risk, namely phenotypic traits that can predispose or protect individuals to disease. The availability of large amounts of GWAS data affords the opportunity to investigate the relationship between myriad traits.1

Unraveling the genetic complexity of Alzheimer disease with Mendelian Randomization