Thus, while there are studies that appear to have shown prelamin A accumulation in peripheral subcutaneous adipose tissue in patients with FPLD2 [14], a more recent study, using an anti-prelamin A monoclonal antibody, did not find such accumulation in cultured fibroblasts from FPLD patients with different variants in the LMNA gene [191]. Here, LMNA is linked to familial partial lipodystrophy, Dunnigan type.