PARPi-sustained IFN-I release in the TME also promotes other relevant immune functions; it activates dendritic cells, sustains cross-presentation of tumor-derived antigens to T cells, is required for NK-cell mediated antitumor immunity, and, in synergy with TLR4 ligands, such as HMGB1, activates M1 antitumor macrophages [106,107]. Here, HMGB1 is linked to neoplasm.