To determine if activation of OAS2 by a future breast cancer therapeutic could provide a new therapeutic strategy, and to distinguish OAS activation from that of TLR3, we combined the Oas2 mutation with expression of the polyoma middle T oncogene (PyMT) driven by the mouse mammary tumor virus promoter (MMTV) [25] and asked if this altered the initiation or progression of mammary cancer, and the interaction with checkpoint immunotherapy. Here, TLR3 is linked to breast cancer.