In addition to albumin, the glycocalyx degradation during sepsis contributes to the non-selective leakage of other mid-sized plasma proteins, including endogenous anticoagulants such as antithrombin and protein C. This loss, secondary to the endothelial junction disruption, may further exacerbate coagulopathy and microvascular thrombosis [23,24]. This evidence concerns the gene ALB and Sepsis.