Indeed, R482W (familial partial lipodystrophy, FPLD) mutant lamin was shown to behave like the wild-type counterpart; an increased mobility within nuclear lamina was observed in L85R (DCM) and L530P (autosomal dominant Emery-Dreifuss muscular dystrophy) mutants. This evidence concerns the gene LMNA and familial dilated cardiomyopathy.