It has also been reported that most FPLD2 patients with the previously described classic phenotype are those who harbour heterozygous missense variants affecting arginine at codon 482 in exon 8 of the LMNA gene, while those presenting with other LMNA variants are considered to have atypical FPLD2. This evidence concerns the gene LMNA and familial partial lipodystrophy, Dunnigan type.