Supporting the involvement of both elements, P2X7R and TNAP, in AD-associated pathology, it was also reported that (i) AD patients and mouse models mimicking this disease present both proteins with altered expression levels and function [17,18,23], and (ii) the genetic ablation or selective pharmacological blockage of each of these targets reverts AD-associated behavioral deficits and elongates the life expectancy of different mouse models mimicking this disease [16,17,18,23]. The gene discussed is ALPL; the disease is Alzheimer disease.