Despite these suitable premises, the development of LXR agonists as therapeutic agents has been hindered by various side effects, including increased hepatic lipogenesis and consequent steatosis, hypertriglyceridemia, and neuroinflammation, most of which are attributed to systemic and/or liver-specific activation of LXRα [24]. The gene discussed is NR1H3; the disease is hypertriglyceridemia.