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The lactate accumulation driven by the Warburg effect not only alters the acid-base balance of the tumor microenvironment, but more importantly, serves as a precursor initiating protein lactylation modification ( Figure 1 3.1 The distinct positioning of lactylation within the landscape of metabolism-derived PTMs Tumor metabolic reprogramming drives diverse post-translational modifications derived from metabolic intermediates, including acetylation (acetyl-CoA-dependent), succinylation (succinyl-CoA-dependent), crotonylation (crotonyl-CoA-dependent), and lactylation (lactate-dependent) ( This shared enzymatic machinery raises a central question: in the context of tumor therapeutic resistance, why focus on lactylation rather than other metabolism-driven acylation modifications
