LMNA and Hutchinson-Gilford progeria syndrome: The efficacy of an antisense curative access involving morpholino antisense oligonucleotides (AON) in spatially limiting the atypical LMNA splicing section that leads to producing progerin protein has previously been demonstrated ex vivo on cells obtained from HGPS patients and in vivo on a knock-in LmnaG609G/G609G mouse model [67].