Many of the downstream events that result in abnormal survival of RA-FLS are dysregulated by constitutive as well as cytokine and growth factor-induced activation of Janus Kinase-Signal Transducers and Activators of Transcription (JAKTAT) [36,37,38,39,40], Stress-Activated Protein Kinase/Mitogen-Activated Protein Kinase (SAPK/MAPK) [40,41,42,43] and PI3K/Akt/Phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/mechanistic target of rapamycin (mTOR) signaling [10,44,45,46,47,48,49] signaling pathways which regulate the balance between cell survival and apoptosis. This evidence concerns the gene MTOR and rheumatoid arthritis.