BACE1 and Alzheimer disease: We gave priority to the SEZ6(R615H) variant among those reported in Table 1, considering that SEZ6 has already been reported as relevant for molecular mechanisms involved in AD pathogenesis, because it is a substrate of the BACE-1 enzyme (β-secretase), affects synapse formation, and is reduced in the cerebrospinal fluid of patients with AD, as revealed by a proteomic study [23–25].