In addition to summarizing the classic mechanisms underlying PD‐1/PD‐L1 blockade enhancement, a few cutting‐edge mechanisms for overcoming resistance to anti‐PD‐1/PD‐L1 therapy by IFN‐α/β are discussed in this review, including stimulation of the cGAS‐STING‐IFN‐I axis, activation of tumor immunogenicity and immune cells, modulation of the TME, induction of ICD, and upregulation of PD‐L1 expression. Here, CGAS is linked to neoplasm.