We generated graded levels of mutations for Hh signaling by introducingthe Alx4Lst allele into a Gli3Xt/Xtbackground, and analyzed the resultant compound mutant embryos at E18.5 (Fig. 3A–D,A'–D').The physiological umbilical hernia was recovered, and pubic symphysis wasformed in wild-type embryos at E18.5 (Fig.1D,I and Fig. 3A,A').Decreasing wild-type Alx4 alleles accelerated the degreeof omphalocele in the Gli3Xt/Xt embryos (Fig. 3B–D). This evidence concerns the gene ALX4 and Umbilical hernia.