Indeed loss of Cyclin D1 in over-expressing miR-199b-5p clones are a reminder of the similar effects seen in Ccnd1–/– mice, which have decreased early GNP proliferation and early ataxia as a consequence of a delay in acquiring normal cerebellar function, thus affecting progression of the pre-neoplastic lesions to MBs [43]. The gene discussed is CCND1; the disease is cerebellar ataxia.