CD8A and neoplasm: Once in the TME, liposomal STING agonists were released through hyaluronidase‐mediated cleavage, augmenting the cellular internalization of STING agonists by tumor cells.[72] As a result, NEs@STING‐Mal‐NP treatment significantly increased the infiltration of macrophages, DCs, NEs, and CD8+ T cells, reinvigorating the immunosuppressive microenvironment of TNBC.[72] Remarkably, the combination of NEs@STING‐Mal‐NP with an anti‐PD‐1 antibody achieved a tumor inhibition rate of approximately 90.6%, a dramatic improvement over αPD‐1 monotherapy.