A large body of literature strongly supports the key role of the IFNAR signaling pathway in controlling anticancer immunosurveillance, and dictating the success of chemotherapy and radiotherapy-induced immune responses, even against MHC class I-deficient tumors that are innately resistant to PD-1 blockade.34–37 The expression of IFNAR1 was comparable between the MCA205, MC38 and AT3 tumor cell lines (Supplementary information, Fig. S3). Here, PDCD1 is linked to neoplasm.