Although the molecular mechanism underlying EC-driven crosstalk with cancer cells has not been elucidated and requires further studies, we can speculate that TRPC3-mediated Ca2+ signaling in TECs may promote the release of growth factors or chemokines, which in turn promote cancer cell migration, as Ca2+ signals are known as key players in EC activation in the tumor microenvironment, one of the most relevant steps in tumor progression [4,39]. Here, TRPC3 is linked to neoplasm.