■Decreased IL-1β and S100A8 expression, improving Cftr-knockout mice’s ability to combat P. aeruginosa lung infection [52];■Arachidonic acid downregulation and increased levels of docosahexaenoic acid in CF patients [53];■Reduced IL-1β, IL-6, and PGE2 pro-inflammatory cytokine expression via suppression of JAK-STAT, PI3K-Akt, PKC, and downstream NF-κB signaling pathways in A. actinomycetemcomitans-infected murine monocyte/macrophage [80]. This evidence concerns the gene CFTR and cystic fibrosis.