The impaired transcriptional response to the canonical Wnt ligand, Wnt3A, in GRK2−/−cells, was accompanied by downregulated LRP6 expression and markedly diminished phosphorylation of PPPS/TP motifs within the LRP6 cytoplasmic tail, demonstrating that defective canonical Wnt signaling also contributes to the ATD phenotype. This evidence concerns the gene WNT3A and Jeune syndrome.