Furthermore, Aβ42 oligomer-mediated activation of the β2-adrenergic receptor results in the β-arrestin-dependent activation of ERK1/2 and genetic deletion of the β2-adrenergic receptor ameliorates the pathophysiological deficits associated with the APPswe/PS1ΔE9 mouse model of AD [50]. The gene discussed is MAPK3; the disease is Alzheimer disease.