In a rodent model of sepsis, we demonstrated that PKCδ was activated in the lung endothelium, and selective PKCδ inhibition with a specific PKCδ-TAT peptide inhibitor attenuated neutrophil influx into the lung, decreased ICAM-1 and VCAM-1 expression, reduced alveolar-capillary permeability, decreased pulmonary edema, and preserved lung architecture [149,150,151,152]. The gene discussed is PRKCD; the disease is Sepsis.