High levels of TNF and interleukin-1β in hepatic environment can negatively regulate APOA1 gene expression via nuclear receptors LXRs (liver X receptor), FXRs (farnesoid X receptor) and PPARα (peroxisome proliferator-activated receptor α) in hepatocytes [97–99], and maybe leading the modulation on ApoA-I expression in leprosy patients. The gene discussed is NR1H4; the disease is leprosy.