Taken together, these data support the conclusion that a stoichiometric interaction between CD44 and RHAMM on the membrane is required to initiate invasive behaviors of cancer cells, and that an imbalance between the two may abrogate cancer cell metastatic potential, at least in part through the inhibition of filopod formation that arises, in turn, from the inactivation or mislocalization of RHAMM. This evidence concerns the gene CD44 and cancer.