While both the isoflurane and Propofol groups exhibited an upregulation in HIF-1 with exposure to sepsis, only the isoflurane group exhibited upregulation in HO-1 [an anti-oxidant protein that produces carbon monoxide and initiates mitochondrial biogenesis (47)], iNOS [an enzyme that produces the free radical NO under conditions of oxidative stress, and which is known to be hepatotoxic (48)], and bcl-2 [a key regulator of mitochondrial autophagy, which inhibits beclin-1 (49)]. The gene discussed is BCL2; the disease is Sepsis.