Based on these observations, our study revealed that PML-RARα interacts with PPARγ to disrupt the PPARγ/RXR heterodimer and promote PPARγ ubiquitination and degradation, which may partially explain the obesity and dyslipidemia in newly diagnosed patients with APL that is driven by PML-RARα. The gene discussed is PPARG; the disease is obesity due to melanocortin 4 receptor deficiency.