These findings are consistent with preclinical evidence of sex and APOE4 effects on brain mitochondrial deficits in animal models (Djordjevic et al., 2020), and translational studies of midlife individuals at risk for AD (Mosconi et al., 2017, 2018a,b, 2021; Rahman et al., 2020). The gene discussed is APOE; the disease is Alzheimer disease.