One key phenomenon in both Alzheimer’s Disease and RBC responses to hypoxia involves protein isoaspartyl-damage arising from dehydration/deamidation-triggering oxidant challenges (e.g., to structural proteins like 4.1 and band 3 in the aging RBC; to tau protein in Alzheimer’s disease), a process that is, in part, counteracted by protein L-isoaspartyl O-methyltransferase both in RBCs and neural cells (D’Alessandro et al., 2023b). The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.