Mechanistically, BPA disrupts hepatic lipid homeostasis through two distinct mechanisms: (1) estrogen receptor (ER) antagonism, impairing lipid oxidation and promoting ectopic fat deposition (9, 10), and (2) NLRP3 inflammasome activation, driving pro-inflammatory cytokine release (e.g., TNF-α, IL-1β, and IL-6) that exacerbates hepatic insulin resistance (11, 12). The gene discussed is ESR1; the disease is Insulin resistance.