In vitro leptin exposure enhanced CCL2 expression/secretion and increased KDM6A/KDM6B and EP300 transcription, highlighting how obesity‐driven epigenetic mechanisms, including leptin‐mediated pathways, disrupt ASC plasticity and perpetuate adipose tissue dysfunction, offering novel therapeutic targets for metabolic disease intervention. The gene discussed is KDM6A; the disease is Other metabolic disease.