Critically, ADNVs treatment caused a remarkable shift of TME to an inflamed and tumor-unfavorable status, characterized by highly expression of pro-inflammatory cytokines, leukocyte-recruiting chemokines, type I interferon (IFN) and IFN-stimulated genes (ISGs), as well as the signature genes related with dendritic cell maturation and T-cell priming (Fig. 3a). Here, IFNA1 is linked to neoplasm.