Chronic inflammation is a well-known tumor-enabling capacity, which allows nascent tumors to acquire all the hallmark capabilities, including the escape from immunosurveillance. Soluble and cellular inflammatory mediators constitute the complex network of the tumor microenvironment, in which tumors grow and with which constantly interact. Myeloid cells (e.g., tumor associated macrophages) are pivotal players of the tumor microenvironment and are characterized by plasticity, which consists of the ability to acquire distinct phenotypes in response to the microenvironment in which they reside. Neutrophils are emerging as important players of tumor microenvironment, given their heterogeneity and plasticity. Increasing evidence suggests a dual role for neutrophils in modulating tumor behavior and highlights the need for a reassessment of neutrophil functions in cancer initiation and progression.