To further validate whether the astrocytic WNT5B–NFATc2–MMP14 axis contributes to HD pathology in vivo, we employed an astrocyte-specific Cre-expressing AAV (AAV-GFAP-Cre) together with Cre-dependent shRNA vectors to selectively knock down Wnt5b, Nfatc2, or Mmp14 in the striatum of an AAV-mHTT (103Q)-induced HD mouse model (Fig. 7a, b). The gene discussed is GFAP; the disease is Huntington disease.