This hypothesis is supported by a recently published work which demonstrates that the severity of neonatal lethal restrictive dermopathy in which there is prelamin A accumulation, is due to the higher expression of prelamin A compared to the accumulation of progerin in HGPS [56] or even much more than the accumulation of prelamin A in LMNA-linked lipodystrophy, which is similar to our model [23]. The gene discussed is LMNA; the disease is restrictive dermopathy.