IFNA4 and neoplasm: We observed that heat-iMVA in PRC2-loss murine tumor cells (AT3 [sgEed], SKP605 [sgEed]) not only triggered type I IFN production (e.g., Ifnb1 and Ifna4) (Figure 8A), but also rescued the PRC2-loss–mediated IFN-γ signaling deficiency, resulting in increased chemokines and Cd274 (Pdl1) expression (Figure 8B).