If iAβ is depleted at mid-life by transient treatment with activators of BACE1 and/or BACE2 (or by any other iAβ–degrading agent), and if the depletion is “deep” enough, de novo accumulating iAβ would not reach the T0 and T1 thresholds within the lifetime of the individual and neither AACD nor AD would occur. The gene discussed is BACE2; the disease is Alzheimer disease.