Similarly, previous studies have reported that, during SLE disease progression, the signaling cascades involving PI3K/AKT, MAPKs (ERK, JNK, p38) and regulators of the nuclear translocation of NF-κB (IκBs) are critically involved in B cell differentiation and the production of autoantibodies [57, 58]. The gene discussed is AKT1; the disease is systemic lupus erythematosus.