This is consistent with data reported in human bladder cancer cells, supporting the notion that c‐Met may have some transcriptional control over Axl expression47; how the loss of βIII‐tubulin potentially reverses this effect, and whether βIII‐tubulin plays a role in regulating phosphorylation of c‐MET requires further investigation. The gene discussed is AXL; the disease is urinary bladder carcinoma.