Moreover, RTN1-C has been shown to interact with Bcl-xL, and this interaction has been shown to change the subcellular localization of Bcl-xL and reduce its anti-apoptotic activity.25 Although RTN1 has been shown to be involved in various cellular processes and disorders, such as cellular trafficking, autoimmune response, apoptosis, Alzheimer’s disease and regulation of ER stress and DNA damage-induced cell death,18 the mechanisms by which RTN1 exerts these effects in the context of cerebral ischemia/reperfusion injury have not yet been characterized. Here, BCL2L1 is linked to early-onset autosomal dominant Alzheimer disease.