Our data add nuance to previous findings indicating that depletion of Ly6G+ neutrophilic myeloid-derived suppressor cells unmasks adaptive immunity (Stromnes et al., 2014), or that ablation of CXCR2+ tumor-associated neutrophils augments IFN-γ+CD8+ T-cell infiltration to potentiate FOLFIRINOX responses in PDAC models (Nywening et al., 2018). The gene discussed is CXCR2; the disease is neoplasm.