Taken together, both transcriptional and epigenetic regulation of human CREM exemplifies differential gene expression between effector and naïve CD4+ T lymphocyte subsets, but also between T lymphocytes from SLE patients and controls, respectively (Figure 1A). In this context, the PP2A:SP-1 pathway and variable meCpG levels of the CREM promoter P1 appear to control basal CREM transcription, whereas promoter P2 is regulated by AP-1 proteins which account for inducible CREM expression following T cell activation.