Whilst we do not fully understand the mechanism/s by which CVA21 acts to boost CTL responses in less permissive tumor cells, it is possible that viral attachment to cell surface DAF (which is expressed by THP-1 and Kasumi-1; data not shown) or ICAM-1 which is expressed, albeit at low levels, facilitates immune activation and subsequent priming of CTLs. Access to blood samples from cancer patients taking part in the STORM (VLA009A) clinical trial (a Phase I dose escalation study of i.v. CVA21) enabled us to explore immune changes that occur in the blood following intravenous delivery of CVA21. The gene discussed is CD55; the disease is cancer.