The fMLP promotes primary neutrophil migration in response to bacterial infection, while LTB4, which is secreted by neutrophils, promotes secondary neutrophil migration.27, 28 Previously, we found that (±)17,18‐EpETE reduced fMLP‐induced pseudopod formation by inhibiting Rac activation in a GPR40‐dependent manner.10 In the current study, we found that BM‐3 17(S),18(R)‐EpETE inhibited both fMLP‐ and LTB4‐induced pseudopod formation, and RvE1 and 18‐HEPE also inhibited both fMLP‐ and LTB4‐induced pseudopod formation. The gene discussed is FPR1; the disease is bacterial infectious disease.