EVA1A facilitates glycolysis in esophageal squamous cell carcinoma to boost PLAU histone lactylation and dampen CD8 + T cell activity

High EVA1A expression enhances glycolysis in ESCC, and the resulting lactate further induces H4K12la lactylation and promotes PLAU expression. This inhibits the anti-tumor activity of CD8⁺ T cells, suggesting that EVA1A has potential as a therapeutic target for ESCC.