Indeed, given the well-established detrimental impact of the excessive C5a on the function of the neutrophils [7,8], the key inflammatory cells in CF, we speculate that the non-cleaving C5a phenotype acquired by the LasR mutants may account for the general dysfunction of neutrophils that predispose toward increased inflammation and reduced bacterial clearance described in CF patients [35]. The gene discussed is C5AR1; the disease is cystic fibrosis.