In addition, many human diseases caused by protein misfolding (4), including Alzheimer’s disease, Parkinson’s disease, and type II diabetes, may benefit from further study of glucosidase I (GI) (3), which is the mammalian homologue of Cwh41p, and its control of protein folding precision as a possible target for new drugs to be used for treatment of these protein misfolding diseases. This evidence concerns the gene MOGS and early-onset autosomal dominant Alzheimer disease.