Genes and pathways, including Wnt and TGF‐β/BMP pathways, play crucial roles in cerebellar development.[27] Overactivation of Wnt/β‐catenin signaling resulted in premature differentiation of GCPs and mice presented with significantly impaired motor coordination and ataxia.[28] The proliferative aspects of Wnt‐induced self‐renewal may be driven by such genes as Ccnd1, Ccnd2. Here, CCND2 is linked to cerebellar ataxia.