It also reduced expression of Lymphocyte function-associated antigen 1 (LFA-1) and CD44 and regulated Jun-N terminal kinase (JNK) in the reduction of the apoptosis of T cells.[65,66] hCDR1 treatment delayed the production of both anti-DNA antibodies and proteinuria, and increased the survival of lupus-prone mice by regulating B cell activating factor (BAFF).[67] Additionally, hCDR1 improved cognitive behavior and brain pathology in lupus mice[68] and downregulated the expression of the indoleamine 2, 3-dioxygenase (IDO) gene, which is increased in SLE patients.[47]. The gene discussed is MAPK8; the disease is systemic lupus erythematosus.