Taking into account that most circulating monocytes are CCR2+ and our data using gene knockouts and pharmacologic blockade in sm-EAN, we speculate that CCL2/CCR2 signaling could drive pathogenic CD14+ CD11b+ CCR2+ monocyte trafficking into the endoneurium at the blood-nerve barrier in AIDP. The gene discussed is ITGAM; the disease is Guillain-Barre syndrome, familial.