On the one hand, the diminished sensitivity to leptin can potentially disrupt the regulation of the adipoinsular axis, thereby exacerbating hyperinsulinemia and IR.[40] On the other hand, hepatic Lepr defect could induce weight gain, liver steatosis, and liver function damage independent of leptin/Lepr signaling from neurohumoral regulation governed by CNS.[41] These metabolic abnormalities could be ameliorated by re‐expressing Lepr.[42] In this study, Lepr was consistently downregulated in the liver of BPA‐exposed paternal generations and their progeny. The gene discussed is LEPR; the disease is Hyperinsulinemia.