In agreement with a study by the Andreadis group, which suggested that ectopic NANOG expression is able to reverse organismal aging in BM-MSCs, our study showed that the ectopic expression of NANOG or the overexpression of PBX1 results in enhanced AKT phosphorylation, increased HF-MSC proliferation, and decreased cellular senescence at early and late passages, followed by a decrease in markers associated with cellular senescence [36], such as p16, p53, and p21. The gene discussed is TP53; the disease is hydrops fetalis.