Activated T cells were reported to secrete IL-10, which induces PD-L1 expression on MDSCs in a STAT3-dependent manner.90 Furthermore, STAT3 activation could induce VEGF production in MDSCs, whereas STAT3 inhibition by the tyrosine-kinase inhibitor sunitinib reduced tumour angiogenesis and MDSC expansion in vivo.91 As mentioned above, VEGF-mediated STAT3 activation leads to further secretion of VEGF and expression of VEGF receptors, thereby supporting MDSC accumulation and tumour growth.50–53,91. The gene discussed is STAT3; the disease is neoplasm.