IRF3 and cancer: These can in turn amplify the immune response through positive feedback loops by binding to the interferon‐α/β receptor (IFNAR), expressed on nucleated cells such as B cells, T cells, or cancer associated fibroblasts (CAFs).[24] Importantly, the absence of STING or IRF3 leads to a diminished anti‐tumoral immune response and reduced responses to checkpoint blockade.[25]