LMNA and autoimmune polyendocrinopathy: To identify pathways altered in progeroid patients’ MSCs, we used induced pluripotent stem cells (hiPSCs) from patients affected with classical Hutchinson–Gilford progeria syndrome (HGPS, c.1824C>T—p.G608G), HGPS-like syndrome (HGPS-L; c.1868C>G—p.T623S) associated with farnesylated prelamin A accumulation, or atypical progeroid syndromes (APS; homozygous c.1583C> T—p.T528M; heterozygous c.1762T>C—p.C588R; compound heterozygous c.1583C>T and c.1619T>C—p.T528M and p.M540T) without progerin accumulation.