Comparison to other mouse models of HGPS shows that LMNAG/G transgenic mice present with a less severe phenotype than LmnaG609G/G609G and LmnaHG/HG mice, which may be attributed to altered molecular interactions between human LMNA/progerin and endogenous murine nuclear proteins, or alternatively, retention of normal functioning of endogenous Lmna in transgenic mice. Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.