These and other studies will be crucial in determining whether Rlip expression or regulation plays a role in the natural etiology of AD, whether Rlip-based interventions could be protective against the progression of AD, or whether the Rlip+/− mouse model should simply be used as a tool with which to study the impacts of elevated oxidative stress on the progression of AD. This evidence concerns the gene RALBP1 and Alzheimer disease.