In this study, we demonstrated the competition with PLCβ1 for binding to TRAX by either GHCer, or tumor-secreted EVs containing GHCer, resulting in the release of the TRAX-sequestered PLCβ1, leading to Ca2+ mobilization in endothelial cells and enhanced angiogenesis in tumor microenvironment. The gene discussed is PLCB1; the disease is neoplasm.