In addition to gene expression and in vitro studies, the key role of the non-canonical Wnt pathway in CLL pathogenesis was confirmed by independent genetic experiments in the Eμ-TCL1 mouse model of CLL [89,90]: Overexpression of ROR1 in B cells promoted disease development [89] whereas the loss of FZD6, another receptor of the non-canonical Wnt pathway highly expressed in the leukemic B cells in this transgenic model of CLL, caused significant delay in the disease development [90]. Here, ROR1 is linked to B-cell chronic lymphocytic leukemia.