Tesson’s group showed that overexpression of mutant lamin C (D192G), which is also associated with DCM, results in the mis-localization and trapping of SUMO1 proteins inside lamin C nuclear aggregates, the phenomenon that was abrogated by the disruption of the SUMO1 di-glycine motif required for SUMOylation [83]. This evidence concerns the gene LMNA and familial dilated cardiomyopathy.