AKT1 and rheumatoid arthritis: Cho et al. (2006) found in mouse experiments that IL-23 binding to its receptor activates JaK2 protein, which in turn activates PI3K/Akt and NF-κB signaling pathways, and the activated PI3K/Akt pathway can also directly stimulate STAT3, resulting in a phosphorylation response that induces IL-17 production. In a study by Kim et al. (2005), they found that an increase in IL-17 expression in activated T cells in RA patients may be a consequence of the activation of PI3K/Akt and NF-κB signaling pathways.