Specifically, if experimental designs such as insertion of microRNA miR-9, SRSF2 siRNA, or splice-switching exon 11 antisense oligonucleotides (ASO E-11) are implemented to increase the lamin C:progerin transcript ratio, pathological phenotypes associated with progeria and aging could be ameliorated by preventing the translation of faulty LMNA mRNA splice variants into progerin (Scaffidi and Misteli, 2005; Jung et al., 2012; Lee et al., 2016). The gene discussed is LMNA; the disease is progeroid syndrome.