Numerous studies have shown that LPS‐induced sepsis may lead to cholestasis by: (i) interfering with: (a) membrane pumps' activity, (b) aquaporins, and (c) nuclear receptors involved in inflammatory responses; (ii) activating LPS/TLR4 and PI3K signaling pathways; (iii) generating a pro‐inflammatory state. The gene discussed is TLR4; the disease is cholestasis.