Pertinent to these findings, the endothelial-specific deletion of TRPV4 recapitulated similar tumor phenotypes in global TRPV4KO mice, and the molecular mechanism appears to be the knockdown of TRPV4 that increases translocation and phosphorylation of VEGFR2 through YAP, which is activated by the Rho/Rho kinase pathway [69,70]. Here, TRPV4 is linked to neoplasm.