Transplantation of HSCs isolated from the progeria mouse model bearing mutation in the gene codifying for the nuclear envelope protein LaminA/C (LmnaG609G/G609G) into healthy recipients did not recapitulate the aged phenotype observed into the progeria mouse model, while chronic treatment with the β3-ADR agonist ameliorated the aged phenotype observed in LmnaG609G/G609G mice, reducing the HSC frequency into the BM. This evidence concerns the gene SUN2 and progeroid syndrome.