Expression and functional analyses of the full set of zebrafish fam20 and xylt genes would test for redundant activities that might compensate for the loss of fam20b and xylt1. We do not expect xylt2 to compensate for a loss of xylt1 function during zebrafish skeletogenesis, because mice deficient for Xylt2 exhibit polycystic kidney disease, but do not have skeletal defects [53]. This evidence concerns the gene FAM20B and polycystic kidney disease.