It has been demonstrated that severe AKI could be protected by targeting the mTOR signaling pathway, the mechanism of which involved inhibiting the apoptosis of tubular epithelial cells (TECs), inducing autophagy, limiting the infiltration of pro-inflammatory cytokines and enriching CD4+CD25+Foxp3+ regulatory T cells in injured tissue.31, 32, 33, 34 However, how mTOR signal regulates MDSCs in the context of AKI was not fully understood so far. The gene discussed is FOXP3; the disease is acute kidney injury.