The forming of capillary tube of HUVECs on Matrigel was used to evaluate the inhibitory effect of cariporide therapy on K562 leukemia driven angiogenesis in vitro. The typical of bloodstream noticed in the tumors based on cariporide met inhibitors group was considerably lower than in control group. These results strongly indicate the inhibitory influence of cariporide on cyst growth and angiogenesis. It’s now recognized that solid cyst growth includes an avascular and a subsequent general phase, all solid tumors progress through both of these stages. It was believed that angiogenesis wouldn’t be as appropriate in these disorders, as lymphatic organs and the bone marrow are prevalent internet sites of tumefaction accumulation in hematological malignancies. Nevertheless, enhanced microvessel density in bone marrow and lymph nodes may be important in providing oxygen and nutrients to the malignant cells, endothelial cell and stromal cells in bone marrow may be important for providing cytokines and growth factors that act on the malignant cells in a paracrine manner to promote their expansion or survival. Accumulative clinical studies show the amount of Immune system angiogenesis or the levels of angiogenic facets are correlated with the level of stage of disease, prognosis or response to therapy. These data strongly declare that angiogenesis induction in hematological cancers has a significance for dis-ease progression. NHE1, that will be ubiquitously expressed and hugely conserved across vertebrate species, plays a significant part in the regulation of intracellular pH and cell volume. Previous studies demonstrate that NHE1 is highly stimulated in myeloid leukemia cell lines to be able to keep an alkaline pHi. Targeted inhibition of NHE1 bring about a reduction in pHi and down-regulation of VEGF in K562 cell line. In this study, we pick a more selective and less cytotoxic NHE1 chemical cariporide to investigate its anti angiogenetic effect. Just-in accordance with previous record, cariporide in a low concentration can result in a decline in pHi and down regulation of VEGF, that was verified by ELISA and western blotting. The focus we used has little effection CHK1 inhibitor on development and growth, hence the big difference on the xenograft cyst size is hypothetically caused by differential angiogenesis. Angiogenesis needs proliferation and migration of endothelial cells. In this study, migration and HUVECs growth was significantly induced by issue medium from K562 cells, which will be 2. 5-times in 1 and proliferation. 5-times in migration, whereas the induction was inhibited by therapy. Cariporide alone did not influence HUVECs, as may be explained by the reduced basal NHE1 activities of endothelial cells.