Tumor-driven activation of STAT3 in neutrophils not only prolongs their survival in tumor tissues but also induces the expression of suppressive molecules for the T cell response, such as PD-L1.11,40,42 This adds another layer of complexity to the cellular sources of this key immune regulatory molecule.43 Since neutrophils are abundant in the tumor microenvironment and play roles in immune modulation, PD-L1 expression on neutrophils could significantly impact the effectiveness of checkpoint inhibitor therapies. This evidence concerns the gene STAT3 and neoplasm.