Patients with POAG and SOAG showed β2-agAAb in >78% of the patients [13, 41] β2-agAAb “hyperactivate” the adrenergic β2-AR in various tissues (e.g. ciliary body, and trabecular meshwork) with consecutive influence on IOP via hypersecretion of aqueous humor and decrease of the outflow facility [12]. Here, ADRB2 is linked to open-angle glaucoma.