More recently, genetic variations in ADAM10 [kuzbanian (kuz) in Drosophila), a protease required for proteolytic cleavage of Notch receptors prior to γ-secretase-dependent cleavage, and TM2D3, a regulator of Notch signaling that has been genetically linked to γ-secretase activity, have been identified as susceptibility loci for the more common late-onset AD through genome-wide and exome-wide association studies [182,183]. This evidence concerns the gene ADAM10 and Alzheimer disease.