The PP2AC subunit was overexpressed in SLE, resulting in the suppression of MAPK/ERK signaling pathway and promoted DNA hypomethylation of CD70, which was involved in the pathogenesis of SLE.135 The increase in PP2AC subunit expression upregulated the production of IL-17 in CD4+ T cells and resulted in more neutrophils in the peripheral blood, thereby promoting inflammation and facilitating the development of SLE.127 Targeting PP2A or its subunit in T cells may therefore be a potential strategy for the treatment of SLE. Here, CD4 is linked to systemic lupus erythematosus.