(A) Inhibition of the Cdc42–STAT3 relationship in cancer. Cdc42 mediated activation of STAT3 is described in various cancer types. Drugs that target Cdc42 including CASIN and MBQ-167 along with shRNA mediated knockdown of Cdc42, have all been shown to induce phenotypic changes in cancer cell lines including the induction of apoptosis, reduced migration and drug sensitivity. (B) Cdc42–STAT3 in pancreatic cell migration. In PANC1 pancreatic cancer cells, IL-6 stimulates JAK2-STAT3 activation via the IL6-R and gp130 co-receptor. STAT3 then relays this activation to Cdc42, an effect exclusive to this Rho-family protein. STAT3-driven activation of Cdc42 involves its interaction with IQGAP1, a scaffold protein, and an additional yet unidentified Cdc42 regulator. Cdc42 is stimulated and catalyses the cellular changes that aid PANC1 cell migration.