Besides the mechanisms so far described, which may be involved at distinct levels in a putatively multi-step progression of the disease, another way in which astrocytes have been recently associated to the pathogenesis of ataxia is through an abnormal anion conductance of GLAST that, although mostly known for glutamate transport, also plays an ancillary function as a chloride channel [103] (Figure 2). Here, SLC1A3 is linked to cerebellar ataxia.