AKT1 and rheumatoid arthritis: Finally, hyperactivation of nuclear factor-κB (NF-κB) and over stimulation of the PI3K/Akt/Protein Kinase B/mammalian target of rapamycin (PI3K/Akt/PKB/mTOR) ‘cell survival’ pathway [24,25,26,27] are also likely to be responsible for the high level of apoptosis-resistance that is typically a characteristic of inflamed RA synovial tissue.