Lamin B, engaged directly in Actin cap formation as anchoring for F-Actin, plays a crucial role in HD nuclear homeostasis; neurons from the HD mouse model showed an increase in Lamin B1 expression, which correlated with nuclear morphology and transport alterations that were restored after Lamin B1 normalization (Figure 4b) [188]. This evidence concerns the gene LMNB1 and Huntington disease.