Several efforts to understand the mechanism of disease in EEC have shown that p63 DBD mutants have both loss their ability to transactivate target genes and also have increased protein stability,22 resulting in a strong dominant-negative effect toward the p63-WT allele.1, 22 As TP63 encodes an essential protein, indispensable to maintain adult stem cells proliferative potential and to engage specific differentiation programs, treatment would necessitate to selectively inhibit the mutant allele expression without affecting WT allele. Here, TP63 is linked to exstrophy-epispadias complex.