We hypothesized that persistent NPCs in postnatal Gdnfhyper/hyper kidneys could either result from general compensatory mechanisms provoked by UB branching defects leading to renal hypoplasia (Kumar et al., 2015; Li et al., 2019) or alternatively derive from the GDNF-specific effects on the NP population. This evidence concerns the gene GDNF and renal hypoplasia.