Preclinical studies demonstrate that targeting lactylation directly or indirectly-through LDH (lactate dehydrogenase) inhibition, MCT blockade, or modulation of lactyltransferases-enhances the efficacy of immune checkpoint inhibitors, Chimeric Antigen Receptor T (CAR-T) therapy, and chemotherapeutic agents.Despite these advances, critical questions remain regarding the specificity of lactylation compared with other post-translational modifications, the tumor types most dependent on lactylation, and reliable biomarkers to guide treatment. Here, SLC16A1 is linked to neoplasm.