Compared to patients with short-term treatment or patients not treated with CDK4/6is for breast cancer, patients who developed acquired resistance to palbociclib exhibited significant activation of the interferon/STAT1 signaling pathway, which induced the expression of immune checkpoints, such as PD-L1, PD-L2, and CTLA-4, on the surface of tumor cells and stromal cells, thereby leading to immunosuppression [86]. This evidence concerns the gene CD274 and neoplasm.