Moreover, following this the importance of ICAM-1 (required for CVA21 infection of tumor cells [24]) on immune cell components was investigated; blockade of ICAM-1 within PBMC, prior to and during CVA21 treatment, completely abrogated the secretion of IFN-α (Fig. 6c) and prevented NK cell activation (no increase in CD69 expression; Fig. 6d) demonstrating a significant role for ICAM-1 in mediating CVA21-induced immune activation. This evidence concerns the gene IFNA2 and neoplasm.