Similar to CD4+ T cell of SLE patients, study on MRL/lpr mice has implied on the role of SIRTI as an important histone acetylation regulator, in which administration of SIRT1-siRNA into the MRL/lpr mice contributes to SIRT1 under-expression, which in turn resulted in the increased levels of global histone H3 and H4 acetylation in CD4+ T cells [85]. This evidence concerns the gene CD4 and systemic lupus erythematosus.