More recently, it has been shown that BACE-1 can also cleave Aβ40 or Aβ42 to generate a C-terminal truncated Aβ34 form, which appears to be a new biomarker of Aβ clearance in AD as it is noticeably increased in mild cognitive impaired patients along with strong BACE-1 activity (Liebsch et al., 2019). The gene discussed is BACE1; the disease is Alzheimer disease.