As discussed in the preceding section, the problem with the employment of the activators of BACE1 and BACE2 in the treatment of conventional AD is that the rate of the influx of iAβ produced independently of AβPP is too great to be matched by the rate of degradation of iAβ by activated BACE1 and/or BACE2. The gene discussed is BACE1; the disease is Alzheimer disease.