The mutation site was introduced into mice through gene targeting, causing the nucleotide at position 1827 of the LMNA gene to mutate from cytosolic deoxyribonucleic acid to thymic dense deoxyribonucleic acid, resulting in the removal of 50 amino acid residues at the end of the pre- lamin A precursor chain base, the truncated prelamin A is called progerin. The progerin retains the CXXA domain while missing the ZMPSTE 24 cleavage site, resulting in the inability to cleave the end of the takin moiety and the persistent presence of exposed farnesylcysteine methylase. The accumulation of progerin can lead to a series of cell defects and dysfunction over time, ultimately leading to aging of cells and tissues and organs.