As shown in Fig. 7, genetic ablation of a single copy of Fgf10 completely rescued the caudal WD phenotype caused by both heterozygous expression of Spry1Y53A and double heterozygous deletion of Spry1 and Spry2, indicating that loss of function of Spry genes cause the caudal WD phenotype at least in part by exacerbating FGF10-mediated downstream signaling. Here, SPRY2 is linked to Wilson disease.