Moreover, neprilysininhibitors used in the treatment of heart failure has been associatedwith an increase in the levels of mitochondrial proteins,28 several of which are downregulated in our studywhere neprilysin levels are enhanced.6 Thesestudies might suggest that the regulation of mitochondrial proteinsis not exclusively mediated by decreased Aβ levels but can alsobe mediated by SST interaction with other proteins and neprilysinoverexpression. This evidence concerns the gene MME and heart failure.