Such is the case of Cyclophilin Cyp60, which drives EMMPRIN from the Golgi to the plasma membrane [18]; the binding to the beta-secreatase components, and the relevance in Alzheimer’s disease [19], or the binding with Caveolins, in which the complexes Caveolin-1/EMMPRIN [7], and Caveolin-3/EMMPRIN in the heart [20] prevent EMMPRIN glycosylation, a step required for EMMPRIN self-aggregation, and downstream-mediated expression of MMPs [21,22]. Here, CAV3 is linked to early-onset autosomal dominant Alzheimer disease.