Considering the significantly overlapping expression patterns of the foxc1 paralogs, it is unsurprising that genetic buffering is observed; this is evidenced by the presence of gut situs defects and an almost complete penetrance of hydrocephalus in foxc1a−/−; foxc1b−/− double homozygotes, which is lacking in both our foxc1a single mutants and those previously published [76]. Here, FOXC1 is linked to Hydrocephalus.