In support of this we have demonstrated that: patient-derived, CVA21-treated PBMC-CM was cytotoxic against AML cell lines (Additional file 6: Figure S4D); IFN-α, which stimulates immune cell activation but abrogates CVA21-direct oncolysis, was induced in CVA21 treated AML patient samples (Additional file 6: Figure S4E); patient NK cells were activated by CVA21 to increase CD69 expression (Additional file 6: Figure S4F); and that NK cell activation correlated with IFN-α production (Pearson’s r = 0.74, p = 0.0009; Additional file 6: Figure S4G). The gene discussed is CD69; the disease is acute myeloid leukemia.