It has been demonstrated that impaired liver synthesis was not the trigger, as hypoalbuminemia occurred within the first 3 days of patients’ admission, far shorter than the half-life of serum albumin, while albumin concentrations were inversely correlated with inflammation markers such as CRP, suggesting that systemic inflammation and capillary leak syndrome was the main pathogenetic mechanism [78]. The gene discussed is ALB; the disease is capillary leak syndrome.