Intriguingly, PARP1 has recently been shown to limit type I IFN secretion by cancer cells with defects in the DNA damage response53,54, and our findings indicate that NAM not only favors type I IFN secretion by TSA cells maintained in vitro, but also (1) elicits signatures of type I IFN signaling in immune cells infiltrating TSA tumors established in immunocompetent hosts, and (2) mediates prophylactic and therapeutic effects that depend (at least in part) on type I IFN responses. The gene discussed is PARP1; the disease is cancer.