This suppression explains why iAβ cannot reach AD pathology-causing levels and, consequently, why the disease does not occur in mouse transgenic models; for these models, it is, more or less, the end of the story (at least as far as the induction of AD or rather the lack thereof is concerned): no matter how extensive the conventional overproduction of Aβ is, it would not reach the AD-causing level due to the “self-suppression” of its production under the ISR conditions and to the lack of the operational AβPP-independent Aβ production pathway. Here, APP is linked to Alzheimer disease.