With respect to the variable potential of plasma samples from different sepsis patients to induce monocyte adhesion, we argued that human endothelial cell-specific molecule-1, a proteoglycan released from endothelial cells under the control of pro-inflammatory cytokines, might interfere with monocyte adhesion via its binding to LFA-1 (CD11a/CD18) on the monocyte surface and blockade of LFA-1 interaction with ICAM-1 [31]. Here, ICAM1 is linked to Sepsis.