We must note that most, if not all, of the EOfAD mutations in APP would appear to have the effect-in-common of increasing expression of APP’s transmembrane C99 fragment (that results from cleavage only at APP’s β-site) and Area-Gomez et al. (2018) have suggested that this may be critical for the increased MAM formation that is the basis of the MAM Hypothesis of Alzheimer’s disease (Schon and Area-Gomez, 2012). The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.