Certainly, STAT3-dependent signal-mediated GBM tumor cells produce more IL-6 thus increasing the level of PD-L1 in immunosuppressive peripheral myeloid cells and facilitating tumor growth (85), which indicates that reciprocal activation of IL-6 and STAT3 continuously fosters chronic inflammation to exacerbate GBM growth and evasion (84). The gene discussed is STAT3; the disease is neoplasm.