The UPRER, when dysregulated by Aβ and tau overexpressions, is also linked to deleterious mitochondrial deficits (Poirier et al., 2019); in the same regard, therapeutic pharmacological targeting of the UPRER has shown concomitant activation of the UPRmt and overall improvement in AD phenotypes (Regitz et al., 2016). The gene discussed is MAPT; the disease is Alzheimer disease.