Likewise, in a murine model of Hutchinson–Gilford progeria (a premature aging syndrome), an increase in the proteosomal degradation of SIRT7 was found due to a destabilization caused by progerin, a partially deleted form of nuclear lamin A. On the contrary, SIRT7 re-expression improved the phenotype and extends life span of these mice [50]. This evidence concerns the gene SIRT7 and premature aging syndrome.