TSNAX and neoplasm: As illustrated in Fig. 5, a novel molecular mechanism for GHCer-induced enhancement of angiogenesis in tumor microenvironment is proposed: GHCer incorporated into endothelial cells via EVs competes with PLCβ1 for binding to TRAX, leading to the dissociation of PLCβ1 from TRAX to induce Ca2+ influx and activation of angiogenesis in tumor microenvironments.