The pro-migratory and pro-invasive role of Endo180 involving the promotion of RhoA-ROCK-based actinomyosin contractility at the cell posterior [17–19] has been confirmed in a range of tumor and stromal cell types, both in vivo and in vitro, using ectopic over expression, genetic silencing, genetic ablation or targeted blockade of receptor function [17–30]. The gene discussed is MRC2; the disease is neoplasm.