Collectively, this and other data suggest that targeted therapies with PARP inhibitors should consider the intended action on aberrant pathways (e.g., directly activated/deactivated by mutations as discussed), but also the accompanying effects such as modulation of the tumor microenvironment (as indicated by changed “inflammatory signatures”), and provide indications for research into combinations of cytotoxic and immunotherapies to increase treatment efficacy. The gene discussed is PARP1; the disease is neoplasm.