The upregulation of PBX1 was further confirmed by dual luciferase assays, as NANOG overexpression significantly increased PBX1 promoter activity, indicating that it might be upstream of PBX1. We performed RNA interference assays to confirm these findings and observed that, as expected, PBX1 knockdown in HF-MSCs that were ectopically expressing NANOG significantly reduced the expression of p-AKT, increased the expression of p16 and p21, and promoted cellular senescence. The gene discussed is NANOG; the disease is hydrops fetalis.