Non-classical HGPS mutations at the exon 11 and intron 11 boundary, including c.1968+1G>A [30] and c.1968+2T>C [31], can also activate the cryptic splice site, leading to the accumulation of progerin and an infantile-onset HGPS phenotype. This evidence concerns the gene LMNA and Hutchinson-Gilford progeria syndrome.