Although effective in other solid tumors, the success of PD-1/PD-L1 immune checkpoint inhibitors and dendritic cell vaccines have been marginal in GB.39–41 Contrary to beliefs that GBs were largely immune-privileged tumors, growing evidence supports robust recruitment of pro-tumor-immune cell populations such as tumor-associated neutrophils and polymorphonuclear myeloid-derived suppressor cells.42,43 Thus, our poorly survived patients with elevated WBC/neutrophil load may underscore these biological mechanisms of tumor progression. The gene discussed is CD274; the disease is neoplasm.