Since microtubule dynamics are required for prostate cancer cell repulsion and EphA, Vav2 and RhoA knockdown prevented ephrin-A5/Fc induced loss of stable and polymerising microtubules, we hypothesised that the failure of CIL we observed in cells treated with EphA, Vav2 or RhoA siRNA could be due to microtubule hyper-stabilisation. The gene discussed is RHOA; the disease is prostate carcinoma.