The second group consists of heterozygous substitution at the junction of exon 11 and intron 11, which activate cryptic splice sites and in-frame deletions including the region of proteolytic site required for the maturation of lamin A. The resultant mutant form of lamin A, termed progerin, is responsible for the Hutchinson-Gilford progeria syndrome and, depending on the level of progerin, a milder form of progeria [8, 9]. Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.