Furthermore, ETI therapy reduced the activation of IL-1 downstream mediators, expression of pro-inflammatory chemokines like CCL3 and CCL4, and reduced the elevated transcription of AQP9 (encoding aquaporin 9), which is involved in IL-1β secretion, in monocyte-derived non-resident macrophages and neutrophils of children with CF [166]. This evidence concerns the gene AQP9 and cystic fibrosis.