The Zic (zinc fingers in cerebellum) family of transcription factors comprises five members, Zic1-5, each of which has five C2H2 zinc finger domains. Fingers 2-5 are >85% conserved across the family, while the first zinc finger domain is unique to each Zic. Zic3 is the only unpaired member of the family and is located on the X chromosome, while the remaining four genes are found in two tightly linked, head to head pairs on two different autosomes (Zic1 plus Zic4 and Zic2 plus Zic5). The five Zic genes are highly conserved from mouse to human and mutant phenotypes have been identified in one or both species for all five genes^[1]. During embryonic development,Zics are broadly expressed in overlapping patterns in the dorsal central nervous system and somites^[2]. This, in conjunction with the high degree of zinc finger domain sequence similarity between the family members, suggests partial compensation of gene function in Zic mutants. Indeed, loss of function of each gene produces a distinct phenotype, but compound mutants may have abnormalities more severe than either single mutant^[3][4]. While all Zic mutants display neural tube defects, additional abnormalities include holoprosencephaly, cerebellar malformation, laterality defects and congenital heart disease^[1].