A study on rodents showed that mice with a THR-α (ThrαPV/PV) mutation had lower hepatic lipid accumulation and decreased lipogenesis, while a negative mutation in THR-β (ThrβPV/PV) led to decreased fatty acid b-oxidation and raised PPARδ signaling, with subsequently increased lipid up-take and liver steatosis [129]. The gene discussed is THRB; the disease is Hepatic steatosis.