Furthermore, in an attempt to discover new mechanisms that could explain the genetic contribution to AD, Jun et al. performed a family-based genome-wide association study in which they identified PlexinA4, a receptor for secreted Sema3A and class 6 (Sema6), as a risk factor in AD pathogenesis or progression by contributing to the acceleration of tau phosphorylation, leading to neurofibrillary tangle formation [130]. This evidence concerns the gene SEMA3A and Alzheimer disease.