In a first phase of the disease, when astrocytes’ reactivity may be protective [76], the inhibition of astroglial NF-κB signaling, likely effective at later stages [58], may indeed result detrimental, while BDNF delivery may delay disease onset fostering astrocytes’ defensive role against neurotoxicity, at least in SCA1 [77]. The gene discussed is BDNF; the disease is spinocerebellar ataxia type 1.