Despite few studies have shown that LPS-induced endotoxemia evokes FAK activation, which contributes to exacerbate the inflammatory response, leading to organ damage and increased mortality (23, 24), so far, no experimental data have been reported on the potential effects of pharmacological modulation of the FAK-Pyk2 signaling pathway against sepsis. This evidence concerns the gene PTK2 and serum lipopolysaccharide activity.