For example, in systemic lupus erythematosus (SLE) model, it was found that PP2Ac transgenic mice produced high levels of IL-17 production from CD4 T cells after induction of glomerular injury [41] and this increased production was later on found to be due to enhanced histone 3 acetylation on the IL-17 locus associated with PP2Ac overexpression [42]. The gene discussed is IL17A; the disease is systemic lupus erythematosus.