The unique pathophysiology of HGPS arises from the distinctive nature of the c.C1824T mutation; despite being a synonymous mutation that does not directly change an amino acid in the lamin A protein, it nonetheless exerts a profound effect on the protein by creating a cryptic splice site that causes incorrect splicing of the LMNA mRNA transcript, resulting in production of a truncated form of lamin A termed progerin, which is constitutively farnesylated. Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.