Notably, disruptions in hPAC precede Aβ overproduction and deposition in various mouse models of AD (Goutagny et al., 2013; Mehak et al., 2022; Victorino et al., 2023), highlighting the close connection between AD-related toxicity and changes in neural network excitability and synchrony, potentially driven by CaMKII signaling dysfunction (Ghosh and Giese, 2015; Imfeld et al., 2013; Opazo et al., 2018; Brown et al., 2022; Brown and Bayer, 2024). The gene discussed is CAMK2G; the disease is Alzheimer disease.