As a synthetic ALX agonist, BML-111 could mitigate inflammatory response in the lung and intestinal mucosal barrier during sepsis by inhibiting the activation of the Akt, ERK1/2, and p38 MAPK signaling pathways and decreasing the expression of TLR2 and TLR4 (Liu H. et al., 2015; Tang et al., 2016). This evidence concerns the gene FPR2 and Sepsis.