Thus, it will be necessary to study the fate of other CB components such as SMN1 in the absence of VRK1 since they might provide clues to its role in the pathogenesis of a complex neurological phenotype associated to VRK1 mutations and that cause a pontocerebellar hypoplasia accompanied by muscular atrophy and ataxia69, 70, 71, 72. This evidence concerns the gene VRK1 and muscular atrophy.