Global population aging has been causing increasing crisis around the world. Hutchinson–Gilford progeria syndrome (HGPS) and Werner syndrome (WS) are two human premature aging disorders with features that closely recapitulate the features of human ageing. Mutations in LMNA and WRN genes lead to aberrant splicing product progerin and protein loss in HGPS and WS, respectively. Study on how genetic alteration leads to the cellular and organismal phenotypes of premature aging will provide clues to the molecular mechanisms that underlie physiological ageing and increased our understanding of molecular pathways contributing to healthy aging. We have generated induced pluripotent stem cells (iPSCs) from fibroblasts obtained from patients with HGPS [1]. Further, using targeted gene correction technology, we successfully corrected the mutated LMNA gene in HGPS-iPSCs [2]. Finally, by using targeted gene “knock-in” technique, we also created WS-specific human embryonic stem cells (hESCs) with WRN mutation as well as Parkinson’s disease (PD)-specific hESCs with LRRK2 mutation [3]. Upon differentiation of these "diseased" human pluripotent stem cells into different somatic cell types, they demonstrated tissue-specific and aging-associated phenotypic defects. Together, these tools offer an unprecedented platform to study the pathogenesis of human aging and aging-related diseases [4].