Some studies using free oxysterols or synthetic LXR agonizts have shown redundancy between LXRα and LXRβ in Abca1 expression, while others, including independent atherosclerosis studies where LXR activation is primarily driven by endogenous ligands, did not see LXRβ compensation under LXRα deficiency, suggesting that there might be differences in responses depending on experimental variables such as the dose, type, or source of the agonizts25,28–31. The gene discussed is ABCA1; the disease is atherosclerosis.