We detail its mechanisms in: (1) Inhibiting antitumor immunity by driving M2 macrophage polarization, enhancing regulatory T cell (Treg) function, and promoting CD8<sup>+</sup> T cell exhaustion; (2) Enhancing intrinsic tumor cell resistance through lactylation-mediated DNA damage repair and stemness maintenance; and (3) Directly undermining immunotherapy, notably by stabilizing programmed cell death 1 ligand 1 (PD-L1). Here, CD274 is linked to neoplasm.