Finally, reprogramming of immunosuppressive myeloid cells (e.g., CSF1R or PI3K-γ inhibitors) can deplete or repolarize tumor-associated macrophages, while blockade of chemokine receptors such as CXCR1/2 or CCR2 reduces the recruitment of myeloid-derived suppressor cells [59,60,61]. This evidence concerns the gene CXCR1 and neoplasm.