Tumors evade the immune system by developing a complex immunosuppressive network that paralyzes the effector arm of the immune system. Tumor immunosuppression is directed by inhibitory cytokines and, more importantly, specific cellular populations. Key parts of this immunosuppressive network are “redirected” myeloid cells (neutrophils and macrophages), “re-educated” by the tumor microenvironment to actually support tumor growth. Neutrophils constitute an important portion of the immune cells infiltrating the tumor microenvironment. Traditionally viewed as the first line of defense against infections, it is now well accepted that neutrophils also have an important role in multiple aspects of cancer biology. Multiple and heterogeneous neutrophil subsets have been identified in tumors and in the circulation. Evidence from many studies including ours now supports the notion that tumor-associated neutrophils (TANs) show functional plasticity driven by multiple factors present in the tumor microenvironment. In my lab, I have been interested in characterizing the different factors modulating the pro-tumor vs. anti-tumor nature of neutrophils in cancer, their functional plasticity, and the mechanisms that regulate neutrophil polarization. Our works on the impact of TANs on other tumor-infiltrating immune cell types such as T cells, have contributed to emphasize the active role of neutrophils as regulators of the immune system, promoting or inhibiting the establishment of a permissive tumor microenvironment. In addition, we have been interested in mapping and functionally characterizing the different circulating neutrophil subpopulations in health and cancer, aiming to understand how manipulating these sub-populations might affect cancer progression.