As an important transcription factor, IRF1 then conversely binds to the IRF1-AS promoter and activates IRF1-AS transcriptional activity, while also elevating the production of IFNs and transcription of many IFN-stimulated genes, ultimately forming a positive regulatory loop that stimulates the IFN response and IFN pathway gene expression to elicit a tumor-suppressive role in ESCC [96]. This evidence concerns the gene IFNA1 and neoplasm.