In their study, Espejel and colleagues investigated the potential for fibroblast-derived iPS cells to proliferate and restore liver function in the FAH-deficient liver failure model (18). Mouse embryonic fibroblasts were reprogrammed to become iPS cells using a plasmid method to deliver the reprogramming transcription factors KLF4, OCT4, SOX2, and c-myc. iPS cells were then injected into blastocysts from Fah^–/– mice, resulting in chimeric mice. The injected iPS cells differentiated in vivo to become hepatocytes. Upon withdrawal of NTBC in the postnatal period, Fah^–/– hepatocytes died, resulting in repopulation of the liver by the transplanted iPS cell–derived (wild-type) hepatocytes and restoration of normal liver function. The authors further tested the proliferative capacity of the iPS cell–derived hepatocytes by demonstrating that these cells proliferated in response to partial hepatectomy and repopulated a Fah^–/– liver as efficiently as did wild-type hepatocytes in a competitive repopulation assay.