To search for a putative additional mechanism, we focused on RhoA since it is a downstream effector protein of the β1-integrin/FAK and also a signaling intermediate of other cascades such as G-protein-coupled receptors (GPCRs)-mediated signaling.31,33 For instance, lysophosphatidic acid (LPA) or sphingosine-1-phosphate (S1P) promotes dephosphorylation and protein stability of YAP1/TAZ by activating RhoA.31 Based upon these, we introduced a constitutively active form of RhoA, namely RhoAQ63L,31 into cancer cells to test if VASP influenced RhoA-induced activation of YAP1/TAZ. This evidence concerns the gene PTK2 and cancer.