CCR2 and neoplasm: Given that systemic neutrophilic silencing is not only clinically impractical, but also drives a compensatory and dynamic myelopoiesis (e.g. of CCR2+ macrophages) that thwarts anti-tumor immunity (Nywening et al., 2018), the chemosensitizing and immune-potentiating effects of NLR attenuation in our model may be related to the disruption of specific tolerogenic functions inherent to tumor-associated neutrophils.