Du et al. demonstrate that AARS1-mediated STAT1 K193 lactylation blocks JAK2 binding and STAT1 phosphorylation, which impairs IFN-γ signaling, reducing chemokine expression and promoting immune escape. Inhibition of this modification with the cell-penetrating peptide K193-pe restores IFN-γ responsiveness, enhances CD8+ T cell recruitment, and improves immune checkpoint therapy efficacy.