Surprisingly both activating and inactivating mutations in RET were identified but no convincing mutations were found in the genes encoding a co-receptor of RET, GFRA, or their ligand, GDNF. These genes became strong candidates for BRAHD following the identification of renal agenesis as a prominent feature in mouse embryos with targeted inactivation of the loci [20]–[22]. Here, RET is linked to renal agenesis.