This relationship can also be observed between cells and cells as exemplified by the imbalance of Th17/Treg in SLE patients [52, 56, 57], and this imbalance is also indirectly observed in our hotspots: the CCR5 encoding a membrane molecule in Foxp3+ Treg was hypermethylated, but the demethylated CCL2 was able to enhance a systemic immune response in proinflammatory cells [58] (Figure 4(c)). Here, FOXP3 is linked to systemic lupus erythematosus.