ROS can activate several pro‐inflammatory signaling pathways, such as AKT and NF‐κB.[22] Stimulation of RA‐FLSs with TNF‐α can rapidly increase the expression of PI3K (p110β) and the phosphorylation of AKT, NF‐κB, and IKK α/β, whereas treatment with LACK156‐173 alleviates the stimulatory effect of TNF‐α on these pro‐inflammatory signaling pathways (Figure 3F,G). The gene discussed is TNF; the disease is rheumatoid arthritis.