It was reported that HO-1-induced excessive generation of CO led to an immoderate dilation of liver sinusoidal and attendant liver failure, whereas the administration of HO inhibitors (Sn-PP and Zn-PP) significantly alleviated sepsis-induced liver injury, as evidenced by lower plasma aspartate aminotransferase and lower liver cyclic guanosine monophosphate, as well as promoted the survival of rats (61.5% and 66.7% vs. 26.7%) [133]. This evidence concerns the gene HMOX1 and liver failure.