Inputs derived from ET-1R promote the formation of a signaling platform containing β-arr1-hMENA/hMENAΔv6/PDZ-RhoGEF converging on RhoC pathway, favoring pericellular matrix degradation, and conferring also a fitness advantage to tumor cells to breach the endothelial barrier and start the transendothelial migration process (Di Modugno et al., 2018). Here, RHOC is linked to neoplasm.