Using an adeno-associated virus (AAV)-based approach to drive astrocyte-specific AQP4 overexpression, we recapitulate the distribution of AQP4 to astroglial fine processes and observe that this change does not impair glymphatic function or alter Aβ levels in the Tg2576 mouse model of amyloidosis [23]. The gene discussed is AQP4; the disease is amyloidosis.