Recent studies have demonstrated higher levels of IL-17 in a CFTR knockout mouse model compared to wild-type mouse during infection with Pseudomonas aeruginosa resulting in the perpetuation of inflammatory process by neutrophil recruitment suggesting that the absence of CFTR contributes to the inflammation by IL-17 production [30] and which have been also observed in patients with active UC [31]. The gene discussed is CFTR; the disease is infection.