These criteria were based on a number of observations in liver failure patients: 1) irreversible loss of the detoxifying function of albumin in ACLF [7], [8]; 2) significant association between loss of albumin function and mortality risk in ACLF [7], [8]; 3) significant association between infection/endotoxaemia and morbidity and mortality in ACLF and ALF [29], [30], [31]; and 4) increasing evidence to support the role of endotoxin in the innate immune response in ALF, which worsens liver injury and clinical liver failure [14], [15], [26]. This evidence concerns the gene ALB and liver failure.