In Alzheimer’s disease (AD), key pathological features, such as amyloid-beta (Aβ) plaque accumulation [69,70], mitochondrial dysfunction, impaired ER-mitochondria crosstalk [71], and decreased S1R activity, contribute to the cognitive impairment and neurodegeneration observed in pathology [72]. The gene discussed is TMBIM4; the disease is early-onset autosomal dominant Alzheimer disease.