Therefore, we hypothesized that increased lamin B1 protein levels in HD brain could be the result of different altered post‐translational mechanisms such as decreased PKCδ (Rué et al, 2014) and/or altered autophagy‐mediated lamin B1 degradation (Dou et al, 2015) and/or increased stabilization due to overactivation of p38MAPK (Barascu et al, 2012). The gene discussed is PRKCD; the disease is Huntington disease.