LMNA and Hutchinson-Gilford progeria syndrome: Structural analyses have suggested the presence of missense and splicing mutations in LMNA-conserved residues [19] which principally affect exon 11 in this gene and correspond to the heptad repeat region of lamin A. Some substitutions do not change the amino acids but lead to the weak activation of the same cryptic splicing site, like in Hutchinson-Gilford progeria syndromes.