AKT1 and cystic fibrosis: Concerning indirect modulations, high levels of miR-155 in CF cells inhibited the translation of the gene SH-2 containing inositol 5’ polyphosphatase 1 (SHIP1), thus leading to the activation of the signaling pathway mediated by phosphatidylinositol-3 kinase/protein kinase B (PI3K/AKT) and the consequent secretion of IL-8 [77].