In mouse models of TNBC, anthracycline-based chemotherapeutic response has been demonstrated reliant on tumor inherent type I IFN signaling and induction.30,31 Further, the presence of a type I IFN metagene predicted complete response to neoadjuvant anthracycline-based therapy in patients with TNBC.30 This link between IFNs and therapeutic response has also been explored in the immunotherapy context in melanoma, where the presence of a type I IFN signature was associated with response to anti-PD-1,32 a checkpoint inhibitor being met with limited success as a single agent in TNBC. Here, PDCD1 is linked to neoplasm.