The efficiency of AON in blocking the aberrant LMNA splicing leading to Progerin production has been previously proven in vitro on classical HGPS patient’s cells and in vivo on a knock-in mouse model (LmnaG609G/G609G) closely mimicking Hutchinson-Gilford Progeria [25]. The gene discussed is LMNA; the disease is Hutchinson-Gilford progeria syndrome.