Not only does the asymmetric RNA-dependent amplification of human AβPP mRNA explain the AβPP-independent production of C100/C99 in Alzheimer’s disease, it also explicates why neither mice nor even long-living mammalian species, such as elephants, develop AD, and why the asymmetric amplification of human AβPP mRNA expressed exogenously from human transgenes is inoperative in animal transgenic models. The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.