Genetic ablation of caspase-1 function in wobbly mice not only reinforced the role of NLRP3 in the progression of neurodegeneration, but also identified caspase-1 as a potential therapeutic target in gliosis-associated ataxias in addition to NLRP3 itself (Fig. 8c, d). Here, NLRP3 is linked to cerebellar ataxia.