The molecular mechanisms by which TRPV4 interacts with actin via Cdc42/N-wasp to alter glioblastoma protrusions, the use of a stable TRPV4 knockdown system and the development of pharmacological inhibitors (GSK2193874) of TRPV4 will lead to a premising therapeutic agent for anti-invasion in human glioblastoma. Here, CDC42 is linked to glioblastoma.