LMNA and familial partial lipodystrophy, Dunnigan type: In fact, the mutation was associated with failure in processing of prelamin A which resulted in accumulation of nonfarnesylated mutated prelamin A. It was further shown that there is a relationship between mutated prelamin A accumulation and the severity of the phenotypes in homozygous familial partial lipodystrophy type 2 patients who harbor the LMNA T655fsX49 mutation [18] (Table 1).