Cancers promote immunological stresses that induce alterations of the myelopoietic output, defined as emergency myelopoiesis, which lead to the generation of different myeloid populations endowed with tumor-promoting activities. New evidence indicates that acquisition of this tumor-promoting phenotype by myeloid cells is the result of a multistep process, encompassing initial events originating into the bone marrow and later steps operating in the tumor microenvironment. The careful characterization of these sequential mechanisms is likely to offer new potential therapeutic opportunities. Here, we describe relevant mechanisms of myeloid cells reprogramming that instate immune dysfunctions and limit effective responses to anticancer therapy and discuss the influence that metabolic events, as well as chemotherapy, elicit on such events.