In favour of this hypothesis, genetic inactivation of Myd88, a critical signal transduction component in TLR signalling and important for downstream IKK/NF-κB activation, alters neuroinflammation and attenuates Purkinje cell loss in a spinocerebellar ataxia type 6 mouse model [37]. This evidence concerns the gene NFKB1 and spinocerebellar ataxia type 6.