Other studies using mice in which the TNF-receptor 1 (TNF-R1) was removed (i.e., TNF-R1 knockout mice) and that were treated continuously with alcohol for 4 weeks determined that the alcohol-induced presence of LPS in the blood (i.e., endotoxemia) led to the release of TNFα from Kupffer cells, that in turn played a direct role in ALD (Yin et al. 1999). Here, TNFRSF1A is linked to serum lipopolysaccharide activity.