We previously reported that soybean oil–based lipid emulsions in PN i.v. solutions in mice led to increased hepatic macrophage recruitment, cytokine production, and hepatocyte apoptosis, followed by the suppression of FXR signaling, and subsequently the onset of hepatic injury and cholestasis,6,7,36 all of which were prevented by treatment with an i.v. FXR agonist.7 On the basis of the results described above, we hypothesized that the FXR agonist-induced hepatic protection in PNAC may have been mediated through activation of IL-6-STAT3 signaling. The gene discussed is STAT3; the disease is cholestasis.