Low BLVRA activity has been demonstrated in an in vivo model of AD, where the reduction of BLVRA activity resulted in not only an increase in BACE1 phosphorylation (BACE1: beta-secretase 1, also known as beta-site amyloid precursor protein cleaving enzyme 1), which increased the Aβ deposits, but also in the induction of insulin resistance by down-regulating the insulin receptor (IR) and inhibiting insulin receptor substrate 1 (IRS1—illustrated in Figure 3), supporting the link between insulin resistance and AD pathology [69,70]. The gene discussed is INSR; the disease is Alzheimer disease.