Previously, it has been revealed that early exposure to Aβ1–42 disrupts the TIP60 HAT/HADC2 balance during the early neurodegenerative stage, while the increase in TIP60 HAT level can significantly improve AD pathology, including Aβ plaque accumulation, neuronal cell death, cognitive deficits, and reduced lifespan, preventing Aβ1–42‐induced transcriptomic changes [12]. The gene discussed is TMPRSS11D; the disease is Alzheimer disease.