Abstract: To explore the role of receptors of the Wnt signaling pathway ( Frizzled/LRP and ROR2 ) in the pathogenesis of leukemia. Methods: Subgrouping of the experiment groups were as follows: Experiment Group 1, bone marrow with acute lymphocyte leukemia ( ALL ); Control Group 1, bone marrow with idiopathic thrombocytopenic purpura ( ITP ); Experiment Group 2: Jurkat, K562, and HL-60 cell lines treated with LiCl; and Control Group 2: Jurkat, K562, and HL-60 cell lines. The expression of the Frizzled-5 and ROR2 receptors in the leukemia cells were detected by reverse transcriptase polymerase chain reaction and Western blot analysis. An MTT assay was used to determine cell proliferation, whereas flow cytometry was used to measure the cell cycle. Results: Fz-2, LRP-6, and ROR2 were expressed in all of the leukemia cells. ROR2 expression was lower in the HL-60 cells than in other leukemia cells. There were no differences in expression with the receptors in other groups. For the 11 ITP bone marrow preparations, ROR2 expression was only seen in 2 of the preparations. No significant differences were found in Fz receptor expression between the ITP and leukemia cells. After the LiCl treatment of the cells, ROR2 expression was obviously lower in the Jurkat cells than in the untreated leukemia cells, whereas no significant differences were found in the expression of the other receptors. The results of the repeated MTT assay showed that LiCl inhibited the proliferation of the three leukemia cell lines in a dose-dependent manner. Comparison of the cell cycles of the Jurkat and HL-60 cells with the normal controls after treatment with LiCl revealed that the proportion of Dip G1 and Dip S decreased and that of G2 increased, with a G2/M block. There were statistically significant differences between the groups ( P < 0.05 ). There were no significant differences in the cell cycle of the K562 cells between the groups treated with varying concentrations. Conclusion: ROR2 expression is higher in ALL cells than in ITP cells. LiCl might affect ROR2 expression in Jurkat cells, and inhibit cell proliferation of leukemic cells, which may suggest that ROR2 is related to the pathogenesis of ALL.