AKT1 and rheumatoid arthritis: Finally, hyperactivation of NF-κB and overstimulation of the Phosphoinositide 3-kinases (PI3K)/Akt/Protein Kinase B/mammalian target of rapamycin (PI3K/Akt/PKB/mTOR) “cell survival” pathway are probably responsible for the apoptosis resistance, characteristic for RA inflamed synovial tissue [8].