In this study, we found that treatment of such cultures with the ERK1/2 inhibitor, SCH772984 [26, 27], or cirmtuzumab, inhibited the capacity of Wnt5a to enhance proliferation of the CLL cells, regardless of whether they used unmutated (U) or mutated (M) immunoglobulin heavy-chain variable region genes (IGHV) (Fig. 1b), suggesting that activation of ERK1/2 was required for the enhanced CLL-cell proliferation and that such activation was ROR1-dependent. Here, MAPK3 is linked to B-cell chronic lymphocytic leukemia.