Indeed, in some old reports, the migratory capacity of peripheral blood neutrophils from patients with PCD (PCD PMN) toward N-formylmethionyl-leucyl-phenylalanine (fMLP), leukotriene B4 (LTB4) and complement component 5a (C5a) has been shown to be reduced (6, 7), whereas others reported unaffected chemotaxis of PCD PMN to the bacterial peptide fMLP or rather aspecific stimuli, such as zymosan (8, 9). The gene discussed is FPR1; the disease is primary ciliary dyskinesia.