While the interesting Aβ34 biology of this article directly impacts the design of future studies looking at Aβ turnover and clinical studies involving BACE inhibitors, we anticipate that combining markers of amyloid clearance (Aβ34 measurements) and deposition (well-established Aβ42 measurements in CSF) may provide a more complete biomarker panel to assess AD samples (i.e., early-stage biochemical changes vs. late-stage plaque/tangle pathology). The gene discussed is BACE1; the disease is Alzheimer disease.