AKT1 and systemic lupus erythematosus: Previous studies have delineated several signaling pathways that contributed to the over-reactivity of B cells in SLE, including Janus kinase/signal transducer and activator of transcription (JAK-STAT), B cell receptor/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT), and TLRs (31), although the detailed molecular mechanisms remain to be elucidated.