ROR1 and B-cell chronic lymphocytic leukemia: In contrast, DOCK2 associates with the SH3-binding site that is dependent upon the proline at position 808 of ROR1 and appears unaffected by the 841-position proline-to-alanine substitution, which can impair the capacity of ROR1 to activate RhoA or enhance the migration capacity of CLL cells [19, 47], indicating that DOCK2 is not required for the capacity of Wnt5a to enhance chemokine-directed migration via activation of ROR1.