While inhibition of BACE1 by FA affords the opportunity to mitigate AD pathology, other BACE1 substrates such as the cell adhesion protein P-selectin glycoprotein ligand-1 [48], the APP homolog proteins APP-like protein 1/2 [49], [50], the low density lipoprotein receptor-related protein [51], the β subunit of voltage-gated sodium channels [52], and the control protein of myelination [53], [54] could be indirectly affected by modulation of BACE1 activity. The gene discussed is SELPLG; the disease is Alzheimer disease.