Wang et al. demonstrated that agonists of the small-molecule stimulator of interferon genes effectively reprogramed M2 TAMs into an antitumorigenic state, characterized by the induction of type I IFN responses and the expression of the costimulatory molecule CD86, and that the expression of CD86 could stimulate T cell cross-priming, increasing the sensitivity of BC cells with BRCA1 and BRCA2 mutations to PARPi treatment [231]. The gene discussed is BRCA1; the disease is breast cancer.