Paradoxically, although there was a decrease in canonical interferon pathways in RMC tumor cells after treatment (Fig. 2d), these same tumor cells expressed significantly higher levels of IFNGR1, which encodes the interferon gamma receptor 1 (Fig. 2f), a receptor that is highly expressed on macrophages and monocytes and promotes antigen presentation on non-immune cells, as well as JAK1, a downstream effector of interferon gamma signaling18,19. Here, IFNGR1 is linked to neoplasm.