Taking into account the studies by Xu et al. [30] showing a pivotal role of nmMLCK in activating β2 integrins to promote sepsis-induced lung PMN recruitment in mice, our results are consistent with a model (Fig. 7) wherein nmMLCK activity in EC and PMN induce the expression of ICAM-1 and activation of β2 integrins, respectively to promote EC-PMN interactions and the associated lung vascular inflammation and permeability. This evidence concerns the gene ICAM1 and Sepsis.