In 2005, increased levels of PP2AC mRNA, protein, and catalytic activity were identified in human SLE T cells, but not in cells from other rheumatic diseases, leading to the dephosphorylation of cAMP response element-binding protein (CREB) and limiting interleukin (IL)-2 transcription and production [6]. The gene discussed is IL2; the disease is systemic lupus erythematosus.