Additionally, due to increased ADAR1 in SLE patients, Orlowski et al. observed an increase of phosphodiesterase 8A1, which participates in the termination of cyclic nucleotide signaling by hydrolyzing cAMP and cGMP and is activated by IFN and enhances T-cell adhesion[17]. The gene discussed is ADAR; the disease is systemic lupus erythematosus.