There is a strong rationale in support of this strategy, given that homologous recombination deficient (HRD) tumors show high expression of PD-1, and the preclinical evidence that double-strand DNA break inducing drugs such as PARP inhibitors allow the accumulation of mutations and hence neoantigens, stimulate upregulation of PD-L1 in tumor cells and activate the innate immune system via the STING pathway with type-I interferon production resulting in optimal recruitment of dendritic cells and priming of T effector cells [83]. The gene discussed is CD274; the disease is neoplasm.