Using breast cancer cell lines and mouse xenograft models, Jiao et al. demonstrated that PARPis upregulated PD-L1 expression, associated with GSK3β inactivation [90], and that PD-L1 upregulation by PARPis attenuated the therapeutic efficacy of PARPis via tumor-associated immunosuppression, as well as determining that simultaneous inhibition of PARP and PD-L1 increased sensitivity to PARPi therapy. Here, CD274 is linked to neoplasm.