Although the SAA patients used in this study did not display typical dyskeratosis congenita phenotype or mutations in DKC1, TINF2, TERT or TERC genes by exome sequencing analysis (Supplementary Tables 2 and 3), we decided to investigate the telomere dynamics in our SAA-iPSC model since it has been reported that one third of acquired AA patients present short telomeres in leukocytes24–26. The gene discussed is TINF2; the disease is severe aplastic anemia.