We could efficiently generate a pool of iPSCs that predominantly possessed homozygous mutations in three disease associated genes, KLF1, CDAN1 and FANCA. The FANCA homozygous mutant iPSCs created through base editing successfully recapitulated salient cellular FA phenotypes that had been previously described in FANCA-/- iPSCs. The gene discussed is CDAN1; the disease is Friedreich ataxia.