Chemical inhibition of CFTR activity in healthy human monocytes using an allosteric CFTR inhibitor (CFTRinh-172) induced increased surface expression of CD64 and CD14 while LPS, elevated in patient serum (31, 58) and therefore used as an in vitro proxy for the inflamed CF circulation, caused a trend toward heightened CD11b expression. The gene discussed is FCGR1A; the disease is cystic fibrosis.