As Eya1, and not Six1 expression was altered in betaglycan mutant metanephroi, it is possible to suggest that the influence of betaglycan on downstream Gdnf expression may be elucidated through perturbations to Eya1 expression and not that of Six1. It is also possible that the conserved Six1 expression in betaglycan mutants may be responsible for sufficient Gdnf expression induction to prevent the manifestation of more severe renal phenotypes such as renal agenesis in betaglycan−/− embryos [35]. The gene discussed is TGFBR3; the disease is renal agenesis.