Emerging evidence demonstrates that lactate directly reprograms macrophage function through metabolic and signaling pathways: (1) It sustains efferocytosis capacity by enhancing PFKFB2-mediated glycolysis, enabling macrophages to continuously clear apoptotic cells during inflammation resolution [37]; (2) It suppresses pro-inflammatory responses via GPR81-dependent inhibition of YAP/NF-κB activation [38]; and (3) It accelerates anti-inflammatory M2 polarization through STAT3 phosphorylation, promoting tissue repair as validated in myocardial infarction models [16]. The gene discussed is NFKB1; the disease is myocardial infarction.