Mechanistically, these phenomena can be attributed to the LXR agonists enhancing SIRT1 signaling, thereby boosting the antioxidant level of FOXO1 and resistance to endoplasmic reticulum stress, as well as deacetylating NF-κB, which in turn mitigates sepsis-induced myocardial injury and dysfunction (142). The gene discussed is FOXO1; the disease is Sepsis.