We show that 1) infection leads to phosphorylation of LRP6 which is independent of CagA and VacA, but depends on a functional T4SS, 2) members of the Dvl family, namely Dvl2 and Dvl3, are involved in LRP6 phosphorylation 3) H. pylori-induced nuclear translocation of β-catenin, LEF/TCF transactivation and target gene expression are significantly reduced in cells with a stable knockdown of LRP6, Dvl2, or Dvl3. This evidence concerns the gene S100A8 and infection.