By using gain-of-function technology, we found that activation or inhibition of Wnt and Notch signaling can affect proliferation of EPSCs, differentiation and migration of keratinocytes, and HF regeneration by targeting MYC proto-oncogene, bHLH transcription factor (c-Myc), and Hes1, which ultimately lead to enhanced or delayed wound healing. This evidence concerns the gene MYC and hydrops fetalis.